Can ingesting substances that are produced by the body cause a permanent withering of the organs that produce the substance?

Can ingesting substances that are produced by the body cause a permanent withering of the organs that produce the substance?

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This question is about substances such as insulin and some vitamins that the human body is able to produce on its own.

Some substances that are produced by the body are also present in various body building supplements.

What I wanted to ask is, is there evidence that ingesting these types of substances for prolonged period leads to (permanent?) withering of the organs that produce the substance?

Yes it is possible but in most cases it will not occur as the body simply halts production. The most infamous manifestation of this is in adrenal insufficiency. That's where when we take glucocorticoids (e.g. prednisolone used in management of lots of inflammatory diseases like asthma and autoimmune diseases) for a prolonged period at high dose. This causes the adrenal glands to atrophy (physically shrink) and following this sudden withdrawal can be dangerous for a patient. That's why we always slowly withdraw steroids when a patient has been on them for a long period of time.

Mostly no. For example, if a non-diabetic person were to be injected with a small amount of insulin, the pancreas would halt its own production of insulin and, if the dose was too large, begin producing glucagon, which stimulates the liver to produce more glucose to match the dose of insulin. If these periodic doses continue, the size of the islets in the pancreas may decrease, but it is always reversible and the beta cell count may return to normal if the doses cease, although it should be noted that a short period of "withdrawal" may occur. The intensity of this withdrawal will depend on how long the supplement was used and what the supplement is.

Mercury poisoning

Mercury poisoning is a type of metal poisoning due to exposure to mercury. [3] Symptoms depend upon the type, dose, method, and duration of exposure. [3] [4] They may include muscle weakness, poor coordination, numbness in the hands and feet, skin rashes, anxiety, memory problems, trouble speaking, trouble hearing, or trouble seeing. [1] High-level exposure to methylmercury is known as Minamata disease. [2] Methylmercury exposure in children may result in acrodynia (pink disease) in which the skin becomes pink and peels. [2] Long-term complications may include kidney problems and decreased intelligence. [2] The effects of long-term low-dose exposure to methylmercury are unclear. [6]

Mercury poisoning
Other namesMercury toxicity, mercury overdose, mercury intoxication, hydrargyria, mercurialism
The bulb of a mercury-in-glass thermometer
SymptomsMuscle weakness, poor coordination, numbness in the hands and feet [1]
ComplicationsKidney problems, decreased intelligence [2]
CausesExposure to mercury [1]
Diagnostic methodDifficult [3]
PreventionDecreasing use of mercury, low mercury diet [4]
MedicationAcute poisoning: dimercaptosuccinic acid (DMSA), dimercaptopropane sulfonate (DMPS) [5]

Forms of mercury exposure include metal, vapor, salt, and organic compound. [3] Most exposure is from eating fish, amalgam-based dental fillings, or exposure at work. [3] In fish, those higher up in the food chain generally have higher levels of mercury, a process known as biomagnification. [3] Less commonly, poisoning may occur as a method of attempted suicide. [3] Human activities that release mercury into the environment include the burning of coal and mining of gold. [4] Tests of the blood, urine, and hair for mercury are available but do not relate well to the amount in the body. [3]

Prevention includes eating a diet low in mercury, removing mercury from medical and other devices, proper disposal of mercury, and not mining further mercury. [4] [2] In those with acute poisoning from inorganic mercury salts, chelation with either dimercaptosuccinic acid (DMSA) or dimercaptopropane sulfonate (DMPS) appears to improve outcomes if given within a few hours of exposure. [5] Chelation for those with long-term exposure is of unclear benefit. [5] In certain communities that survive on fishing, rates of mercury poisoning among children have been as high as 1.7 per 100. [4]

What are magic mushrooms and psilocybin?

Psilocybin is a hallucinogenic substance people ingest from certain types of mushrooms that grow in regions of Europe, South America, Mexico, and the United States.

The mushrooms containing psilocybin are known as magic mushrooms.

According to the United Nations 1971 Convention on Psychotropic Substances, Psilocybin is a Schedule I controlled substance, meaning that it has a high potential for abuse and serves no legitimate medical purpose.

Individuals use psilocybin as a recreational drug. It provides feelings of euphoria and sensory distortion that are common to hallucinogenic drugs, such as LSD.

Researchers at John’s Hopkins Center for Psychedelic and Consciousness Research published a landmark study in 2006 on the safety and positive effects of psilocybin.

In October 2020, Oregon became the first state to legalize psilocybin. This allows for a 2-year period to consider regulatory and prescribing requirements.

Although medical bodies do not consider psilocybin to be an addictive substance, users can experience disturbing hallucinations, anxiety, and panic from using the drug.

Share on Pinterest Psilocybin is a natural hallucinogen. Getty Images

Psilocybin is a hallucinogen that works by activating serotonin receptors, most often in the prefrontal cortex. This part of the brain affects mood, cognition, and perception.

Hallucinogens work in other regions of the brain that regulate arousal and panic responses. Psilocybin does not always cause active visual or auditory hallucinations. Instead, it distorts how some people that use the drug perceive objects and people already in their environment.

The quantity of the drug, past experiences, and expectations of how the experience will take shape can all impact the effects of psilocybin.

After the gut ingests and absorbs psilocybin, the body converts it to psilocyn. The hallucinogenic effects of psilocybin usually occur within 30 minutes of ingestion and last between 4 and 6 hours.

In some individuals, the changes in sensory perception and thought patterns can last for several days.

Mushrooms containing psilocybin are small and usually brown or tan. In the wild, people often mistake mushrooms containing psilocybin for any number of other mushrooms that are poisonous.

People usually consume psilocybin as a brewed tea or prepare it with a food item to mask its bitter taste. Manufacturers also crush dried mushrooms into a powder and prepare them in capsule form. Some people who consume these mushrooms cover them with chocolate.

The potency of a mushroom depends on:

  • the species
  • origin
  • growing conditions
  • harvest period
  • whether a person eats them fresh or dried

The amount of active ingredients in dried mushrooms is about 10 times higher than the amount found in their fresh counterparts.

Extent of use

In the U.S., the National Survey on Drug Use and Health suggested that between 2009 and 2015, around 8.5% of people reported using psilocybin at some point in their life.

The ritual use of psilocybin for mystical or spiritual purposes dates back to pre-Columbian Mesoamerican societies and continues to this day. Psilocybin is often used recreationally at dance clubs or by select groups of people seeking a transcendent spiritual experience.

In medical settings, doctors have tested psilocybin for use in treating cluster headaches, end stage cancer anxiety, depression, and other anxiety disorders.

But some scientists have questioned its effectiveness and safety as a therapeutic measure.

Street names for psilocybin

Drug dealers rarely sell psilocybin under its real name. Instead, the drug may be sold as:


The botulism neurotoxin is one of the most potent, lethal substances known.

  • Botulism is a disease caused by this neurotoxin (specifically A, B, E, or F type neurotoxin) symptoms include a flaccid paralysis (weakness or slackness) in various muscles.
  • Bacteria called Clostridium botulinum produce the neurotoxin.
  • The neurotoxin paralyzes muscles and can be life threatening.
  • There are three major types of human botulism that differ in how they are acquired: foodborne illness, wound, and infant botulism.
  • Eating contaminated home-canned foods can cause foodborne botulism.
  • Never taste-test food that may have gone bad.
  • Wound botulism is due to Clostridium bacteria infecting a wound and releasing the neurotoxin.
  • In infant botulism, the baby consumes spores of the bacteria that then grow in the baby's intestine and release the neurotoxin.
  • Honey can contain botulism spores, and babies less than 1 year of age should not consume it.
  • Effective antitoxin types to block the action of the neurotoxin can treat early foodborne, pediatric, and wound botulism.
  • Botulism neurotoxin is listed as a potential biological weapon.
  • Dilute concentrations of botulism neurotoxin treat medical and cosmetic conditions.

What is botulism?

Botulism is a serious illness that causes flaccid paralysis of muscles. A neurotoxin, generically called botulinum toxin, causes botulism and the bacterium Clostridium botulinum (and rarely by C. butyricum and C. baratii) produces the neurotoxin. There are seven distinct neurotoxins (types A-G) that Clostridium botulinum produces, but types A, B, and E (and rarely F) are the most common that produce the flaccid paralysis in humans. The other types mainly cause disease in animals and birds, which also develop flaccid paralysis. Most Clostridium species produce only one type of neurotoxin however, the effects of A, B, E, or F on humans are essentially the same. Botulism does not spread from person to person. Botulism develops if a person ingests the toxin (or rarely, if it is inhaled or injected) or if the Clostridium spp. organisms grow in the intestines or wounds in the body and toxin is released.

The recorded history of botulism begins in 1735, when the disease was first associated with German sausage (food-borne disease or food poisoning after eating sausage). In 1870, a German physician by the name of Muller derived the name botulism from the Latin word for sausage. Clostridium botulinum bacteria were first isolated in 1895, and a neurotoxin that it produces was isolated in 1944 by Dr. Edward Schantz. From 1949 to the 1950s, the toxin (named BoNT A) was shown to block neuromuscular transmissions in the nervous system by blocking the release of acetylcholine from motor nerve endings. Botulism toxin(s) are some of the most toxic substances known to man while the toxin has been considered for use as a biological weapon, it has also been used to treat many medical conditions. In 1980, Dr. Alan B. Scott used the toxin to treat strabismus (deviation of the eye), and in December 1989, the U.S. Food and Drug Administration (FDA) approved BoNT-A (Botox) for the treatment of strabismus, blepharospasm, and hemifacial spasm in young patients. The use of Botox to treat glabellar lines (wrinkles and frown lines) was approved in 2002 by the FDA for cosmetic improvements the FDA has approved many additional uses (for example, underarm sweating, and muscle pain disorders) since 2002.

In 2017, at least 10 patients were hospitalized with botulism. All of the patients who got botulism ate a nacho cheese sauce served at a gas station near Sacramento, Calif. One patient had to spend at least three weeks in the intensive care unit with paralysis. There is one suspected death due to this botulism outbreak. In 2018, Kraft Heinz produced Taco Bell cheese dip was determined to have a risk of Clostridium contamination. Although no one has developed botulism to date, Kraft Heinz voluntarily recalled about 7,000 cases of the product because of a possible botulism risk.

Botulism Symptoms and Signs

Botulism is a rare, possibly fatal illness linked to improperly canned or preserved foods. Symptoms include cramps, vomiting, breathing problems, difficulty swallowing, double vision, and weakness or paralysis. If you suspect botulism poisoning, call 911.

What causes botulism?

Neurotoxin, synthesized and secreted by Clostridium botulinum bacteria (and a few other Clostridium species), cause botulism. The toxin causes the disease by blocking the release of acetylcholine from motor nerve endings. This result produces the symptoms associated with botulism.

What are risk factors for botulism?

The risk for developing botulism is increased by ingesting foods that may be improperly treated to kill C. botulinum bacteria and their spores (for example, some home-canning methods or a failure in a canning company's production of canned foods like tomatoes or fish) and to denature any toxins. Some honey preparations may contain small amounts of the bacterial spores infants under the age of 1 year are at risk if they are given honey. Corn syrup was once implicated as a cause of botulism in infants, but this was eventually proven not to be the source of toxin. Botulism risk is increased if wounds become contaminated with soil or fecal material.

How many kinds of botulism are there?

There are three main kinds of botulism, which are categorized by how the disease is acquired:

  • Food-borne botulism is caused by eating foods that contain botulinum neurotoxin. Recent small outbreaks have occurred in Canada due to fermented fish and in New York due to unrefrigerated bulk tofu contamination.
  • Wound botulism is caused by a neurotoxin produced within a wound that is infected with the bacteria Clostridium botulinum.
  • Infant botulism occurs when an infant consumes the spores of the botulinum bacteria. The bacterial spores germinate, then grow in the intestines, and release the neurotoxin.

Three other kinds of botulism have been described but are seen rarely.

  • The first is adult intestinal colonization that is seen in older children and adults with abnormal gastrointestinal tracts. Only rarely does intestinal infection with Clostridium botulinum occur in adults because the adult GI tract inactivates ingested Clostridium botulinum bacteria through gastric acid and enzymatic activity. Typically, the adult form of this intestinal botulism is related to abdominal surgical procedures that interfere with such inactivation mechanisms.
  • The second kind (injection botulism) is seen in patients injected with inappropriately high amounts of therapeutic neurotoxin (for example, Botox, Dysport, Myobloc).
  • The third kind (inhalation botulism) has occurred in laboratory personnel who work with the neurotoxins.

All six kinds of botulism are potentially fatal.


How serious is botulism?

Botulinum neurotoxin is considered one of the most potent, lethal substances known. As little as about 1 nanogram/kg can be lethal to an individual, and scientists have estimated that about 1 gram could potentially kill 1 million people. This small amount of toxin capable of killing humans has made the toxin a candidate for use in weapons for biowarfare and bioterrorism. All forms of botulism can be fatal and are considered medical emergencies. Foodborne botulism can be especially dangerous because many people can be poisoned by eating even small amounts of neurotoxin-contaminated food because the toxin is easily absorbed by the digestive system. A botulism outbreak is a public health emergency that is reportable to the U.S. government.

How does botulism neurotoxin affect the body?

A neurotoxin actually paralyzes the nerves so that the muscles cannot contract. This happens when the neurotoxin enters nerve cells and eventually interferes with the release of acetylcholine so the nerve cannot stimulate the muscle to contract. Unless the nerve can regenerate a new axon that has no exposure to the neurotoxin, the interference at the neuromuscular junction is permanent. This is why it takes so long to recover from botulism and also why cosmetic and therapeutic uses of diluted neurotoxin can be effective for relatively lengthy time periods.

What kind of organism is Clostridium botulinum?

Clostridium botulinum is the name of bacteria commonly found in soil all over the world. The bacteria are considered to be anaerobic, which means these organisms grow best in low or absent oxygen levels. Clostridium bacteria are gram-positive rod-shaped bacteria that form spores that allow the bacteria to survive in a dormant state until exposed to conditions that can support growth.

  • There are seven types of botulism neurotoxin designated by the letters A through G.
  • Only types A, B, E, and F cause illness in humans.

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How common is botulism?

Because of better canning processes, especially with home canning or home processing of food, the number of yearly cases of foodborne botulism has dropped to about 1,000 worldwide. In the United States, on average, 110 cases of botulism are reported each year. Of these, nearly 25% of cases are foodborne botulism, approximately 72% are infant botulism, and the remainder (about 3%) are wound botulism, which until recently was rare. Outbreaks of foodborne botulism involving two or more people are usually caused by eating contaminated home canned foods. The number of cases of foodborne and infant botulism has changed little in recent years. However, the incidence of wound botulism has increased, especially in California, from the use of black-tar heroin, which causes infected wounds at heroin injection sites.

What are botulism symptoms and signs?

The classic symptoms of botulism include

    , ,
  • drooping eyelids,
  • slurred speech, , ,
  • muscle weakness (resulting in a flaccid paralysis).

The classic symptoms may also be accompanied by other symptoms and signs such as

  • dilated pupil(s), , , ,
  • abdominal discomfort or pain, , , ,
  • difficulty speaking, , ,
  • slow or absent reflexes, ,
  • facial weakness,
  • eye muscle weakness, and
  • paralysis.

Constipation may occur. The health care professional's examination may reveal that the gag reflex and the deep tendon reflexes like the knee-jerk reflex are decreased or absent.

Infants with botulism appear lethargic, weak, and floppy, feed poorly, become constipated, and have a weak cry and poor muscle tone. In infants, constipation is often the first symptom to occur.

These are all symptoms and signs related to the muscle paralysis that is caused by the bacterial neurotoxin. If untreated, these symptoms and signs may progress to cause paralysis in various parts of the body, often seen as a descending paralysis of the arms, legs, trunk, and breathing muscles that can lead to death.


How soon do botulism symptoms appear?

In foodborne botulism, symptoms generally begin 18-36 hours after eating a contaminated food, but they can occur as early as six hours or as late as 10 days afterward.

What health specialists treat botulism?

In addition to the patient's primary care physician, other health care professionals may be appropriate to consult for example, for hospitalized patients, a critical care specialist, neurologist, infectious-disease specialist, and a pediatric specialist if a child or infant has the disease.

How do health care professionals diagnose botulism?

The patient's history and physical examination may suggest botulism, but these clues are usually not enough to allow a diagnosis of botulism. Symptoms of other diseases, such as a stroke, Guillain-Barré syndrome (another disease of muscle paralysis), and myasthenia gravis (which also causes weakness and eyelid drooping) can appear similar to those of botulism. Special tests may be needed to exclude these other conditions. These tests may include a brain scan, spinal fluid examination, nerve conduction test (electromyography, or EMG), and a Tensilon test for myasthenia gravis. However, if botulism is strongly suspected (for example, several patients with botulism symptoms who ate from the same home-preserved food container), samples should be obtained for a mouse inoculation test (see below) and then the patients should be treated immediately with botulism antiserum. These tests will help distinguish botulism from infections with Salmonella, E. coli, and other Clostridium species (tetani).

The most direct way to confirm the diagnosis is to identify the botulinum neurotoxin in the patient's blood, serum, or stool. This is done by injecting the patient's serum or stool into the peritoneal cavity of mice. An equal amount of serum or stool from the patient is treated with multivalent antitoxin and injected in other mice. If the antitoxin-treated serum- or stool-injected mice live while those injected with untreated serum or stool die, then this is a positive test for botulism and is called the mouse inoculation test. The bacteria can also be isolated from the stool of people with foodborne and infant botulism, but this is not a definitive test. However, stool cultures can help differentiate botulism from E. coli, Salmonella, and other infectious agents.

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What is the treatment for botulism?

If diagnosed early, foodborne and wound botulism can be treated with an antitoxin that blocks the action of neurotoxin circulating in the blood. The trivalent antitoxin (effective against three neurotoxins: A, B, and E) is dispensed from quarantine stations by the U.S. government's Centers for Disease Control and Prevention (CDC). The antitoxin can prevent the disorder from worsening, but recovery still takes many weeks. Another heptavalent antitoxin (effective against seven neurotoxins: A, B, C, D, E, F, and G) may be available from the U.S. Army or FEMA. However, HBAT (botulinum antitoxin, heptavalent) is replacing other antitoxins and is available from the CDC Emergency Operations Center call 770-488-7100 for information and supplies.

Physicians may remove whatever contaminated food is still in the gut by inducing vomiting or by using enemas. Wounds should be treated, usually surgically, to remove the source of the toxin-producing bacteria. Good supportive care (intravenous [IV] fluids, breathing support, for example) in a hospital is the mainstay of therapy for all botulism types.

Enemas may be used to remove unabsorbed toxin however, magnesium salts, citrate, and sulfate are not used as they may add to the toxin's strength. Antibiotics (high-dose IV penicillins or other antibiotics) are not used in foodborne botulism but are used in wound botulism surgical debridement may also be needed. Consultation with an infectious-disease specialist is recommended to help manage treatment protocols.

Antitoxin was not routinely given for the treatment of infant botulism. However, now recommended is the use of BabyBIG (human immune globulin given IV) that is considered safe and effective. Unfortunately, it can only be obtained from the California Department of Public Health (call 510-231-7600), and it reportedly costs $45,300. The respiratory failure and paralysis that occur with severe botulism may require a patient to be on a breathing machine (mechanical ventilator) for weeks and may require intensive medical and nursing care (nasogastric suction, IV augmented nutrition, and Foley catheter, for example). After several weeks, the paralysis slowly improves as axons in the nerves are regenerated.

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What are complications from botulism?

Botulism can result in death from respiratory failure. In the past 50 years, the rate of death from botulism has fallen significantly. Unfortunately, a patient with severe botulism may require not only a breathing machine for ventilation but also intensive medical and nursing care for several months to survive.

Patients who survive an episode of botulism poisoning may experience fatigue and shortness of breath for years, and long-term therapy may be needed to aid recovery.

In 2009, the FDA increased its label precautions on the three available products: Botox, Dysport, and Myobloc. All three are different formulations of the toxin and are not interchangeable with regard to dosing. In addition, the FDA cautions that all the symptoms of botulism can occur if the treatments are inappropriately given, especially in high doses or if some of the solution seeps out of the localized area where it is injected. The FDA further warned health care professionals that suppliers of medical toxins that do not have FDA approval may supply faulty products that could harm individuals.

What is the prognosis of people with botulism?

Untreated botulism has a mortality rate (death rate) of about 50%. Appropriately treated patients with botulism currently still have a mortality rate of about 3%-5%. Some patients may experience various degrees of paralysis for many months. In general, the earlier the diagnosis and treatment of the disease, the better is the prognosis. However, outcomes may be considered only fair in some patients who develop chronic fatigue and shortness of breath for many years after the initial diagnosis and treatment of botulism.

Is it possible to prevent botulism?

Yes, botulism prevention is possible. Foodborne botulism has often come from improperly prepared home canned foods such as asparagus, green beans, beets, and corn. However, there have been outbreaks of botulism from more unusual sources such as chopped garlic in oil, agave nectar, chili peppers, broccoli, tomatoes, tomato sauce, improperly handled baked potatoes wrapped in aluminum foil, and home canned or fermented fish. People who do home canning should follow strict hygienic procedures to prevent or kill Clostridium bacteria, their spores, and neutralize its neurotoxin. Oils that are infused with garlic or herbs should be refrigerated. Potatoes that have been baked while wrapped in aluminum foil should be kept hot until served or refrigerated. Bacon should be cooked well since bacon preservatives (salts), which inhibit clostridial spores, have been reduced. Because botulism neurotoxin is destroyed by high temperatures (85 C for five minutes), people who eat home-canned foods should consider boiling the food for 10 minutes before eating it to help ensure that the food is safe to consume and reduce the possibility of getting food poisoning. Other canned foods that are commercially produced (especially low-acid foods like vegetables, meats, and seafood) and bulging (the can is deformed and looks like it is over-pressurized) or if abnormal-smelling preserved foods are found, they should be discarded. Do not taste-test them or attempt to boil the food!

Because honey can contain spores of Clostridium botulinum and this has been a source of infection for infants, children less than 12 months of age should not be fed honey. Honey is relatively safe for people 1 year of age and older.

Wound botulism can be prevented by promptly seeking medical care for infected wounds or skin cuts and avoiding injectable street drugs.

The FDA publishes recall lists of commercially produced foods that may contain botulinum toxin. One large recall was Castleberry Food Company's hot dog chili sauces and dog food in 2007. In October 2009, Plumb Organics issued a recall of baby food (apple and carrot preparations) that was thought to be tainted with botulinum toxin. In October 2015, Seaquest Seafood Corp., in California, recalled its Sunrise brand marinated fish. Several types were recalled by the FDA due to potential Clostridium botulinum contamination. Several other FDA recalls have occurred in 2015, including one in Ohio due to home canned potatoes that killed one and sickened about 50-60 others. Avoiding such potential sources of toxin can prevent botulism.

Vaccine development for the major human types of botulism neurotoxin is currently being investigated, but there is no vaccine commercially available or approved for public use by the FDA. However, in the United States, an investigational pentavalent (against neurotoxins A, B, C, D, and E) botulinum toxoid vaccine can be distributed by the CDC for laboratory workers at high risk of exposure to botulinum toxin and by the military for protection of troops against attack. Unfortunately, it takes several months to induce immunity. In 2009, a research finding with molecules that mimic botulism toxin binding sites was described that may provide another method to block toxin from binding to nerve tissues, but this approach is only in the research phase of development.

The herb milk thistle has been suggested by alternative medicine proponents (mainly in Europe) to treat food poisoning (especially mushroom poisoning) and to help detoxify the liver. There are no good data on its use in preventing or treating botulism.

Is botulism neurotoxin really considered to be a potential biological weapon?

Yes. However, the neurotoxin rapidly inactivates when exposed to air and is relatively unstable even in liquid formulations in contrast to other disease agents like organisms that cause anthrax. Even with these drawbacks, the neurotoxin has been used sporadically in attempts to harm or kill individuals. Botulinum toxin could be used to contaminate food supplies, but some experts suggest that dissemination of the toxin as an aerosol would be more effective. During the Gulf War, Iraq reportedly produced 20,000 L of botulinum toxin and used 12,000 L for field-testing and to fill warheads, but the shells were not used. The Aum Shinrikyo cult in Japan tried and failed three times to use the toxin as an aerosol weapon. Scientists in Russia also have experimented with botulinum toxin as a weapon. These situations are described in detail in the literature that discusses chemical and biological warfare.

Why are botulism neurotoxins used as cosmetic treatments or treatments for some medical conditions?

Interestingly, purified and highly diluted botulism toxin is being used to treat conditions that are characterized by abnormal muscle contractions. (Some examples of these conditions are torticollis, spasmodic dysphonia, achalasia, strabismus, oromandibular dystonia, cervical dystonia, and blepharospasm.)

Wrinkles are caused by repeated normal muscle contractions. no muscle contractions, no wrinkles. Consequently, many people elect to have an FDA-approved formulation of the dilute toxin injected to reduce or stop wrinkles in the skin. This wrinkle treatment was first approved by the FDA in 2002. Possible side effects of this treatment include bruising, ptosis (abnormal drooping of a body part, especially the eyelid), nausea, and dysphasia (difficulty with speech), but other side effects may also occur. The last reference listed below shows pictures of frown line treatment with Botox.

Some physicians use botulinum toxin type A as a treatment of gastrointestinal complications of diabetes.

Ch. 43 -- Immune System

molecular recognition relies on a small set of receptor proteins that bind to molecules or structures that are absent from animal bodies but common to a group of viruses, bacteria, or other pathogens.

Binding of an innate immune receptor to a foreign molecule activates internal defenses, enabling responses to a very broad range of pathogens.

is activated after the innate response and develops more slowly

molecular recognition relies on a vast arsenal of receptors, each of which recognizes a feature typically found only on a particular part of a particular molecule in a particular pathogen. As a result, recognition and response in adaptive immunity occur with remarkable specificity. HIGH SPECIFICITY -- receptors provide pathogen-specific recognition

enhanced by previous exposure to the infecting pathogen. (e.g synthesis of proteins that inactivate a bacterial toxin and the targeted killing of a virus-infected body cell.)

Hemocytes also secrete antimicrobial peptides that disrupt the plasma membranes of fungi and bacteria carries out phagocytosis (major immune cells in invertebrates)

The immune system recognizes bacteria and fungi by structures on their cell walls

*Innate defenses of mammals are similar to those of invertebrates

skin and mucous membranes of the respiratory, urinary, and reproductive tracts (Mucus traps and allows for the removal of microbes)

Many body fluids including saliva, mucus, and tears are hostile to many microbes

Neutrophils circulate in the blood

Macrophages reside permanently in tissues

Natural killer cells
Detect abnormal cells
Kill abnormal (cancer) or pathogenic cells

produce signals that initiate responses tuned to the invading microorganism.

A type of white blood cell that engulfs invading microbes and contributes to the nonspecific defenses of the body against disease.

Found within the lymph nodes, they are phagocytes that destroy bacteria, cancer cells, and other foreign matter in the lymphatic stream.

Some migrate throughout the body, whereas others reside permanently in organs and tissues where they are likely to encounter pathogens. For example, some macrophages are located in the spleen, where pathogens in the blood are often trapped.

innate and adaptive immunity

antibody-antigen binding complex enhances this type of WBC

mainly populate tissues, such as skin, that contact the environment. They stimulate adaptive immunity against pathogens that they encounter and engulf

constantly surveying for pathogenic/ foreign / abnormal cells

Innate immune cells in mammals detect, devour, and destroy invading pathogens

These cells recognize groups of pathogens using TLRs, or Toll-like receptors

transmembrane protein of immune cells that recognizes pathogens and activates an immune response directed against those pathogens

on host cells attach to pathogen-associated molecular patterns (PAMPs)

A group of about 30 blood proteins that may amplify the inflammatory response, enhance phagocytosis, or directly lyse extracellular pathogens. *CASCADE*

lysis of invading cells
triggers inflammation

tag foreign cells drastically enhances macrophage phagocytosis & immune efficiency

a set of events triggered by signaling molecules released upon injury or infection----> Activated macrophages discharge cytokines, signaling molecules that recruit neutrophils to the site of injury or infection.

Mast cells, immune cells found in connective tissue, release histamine, which triggers blood vessels to dilate and become more permeable

-Activated complement proteins promote further release of histamine, attracting more phagocytic cells
-Enhanced blood flow to the site helps deliver antimicrobial peptides

The result is an accumulation of pus, a fluid rich in white blood cells, dead pathogens, and cell debris from damaged tissues

Inflammation can be either local or systemic (from more extensive tissue damage or infection)---> Cells in injured or infected tissue often secrete molecules that stimulate the release of additional neutrophils from the bone marrow.

Fever is a systemic inflammatory response triggered by substances released by macrophages in response to certain pathogens

How do drugs produce pleasure?

Pleasure or euphoria—the high from drugs—is still poorly understood, but probably involves surges of chemical signaling compounds including the body’s natural opioids (endorphins) and other neurotransmitters in parts of the basal ganglia (the reward circuit). When some drugs are taken, they can cause surges of these neurotransmitters much greater than the smaller bursts naturally produced in association with healthy rewards like eating, hearing or playing music, creative pursuits, or social interaction.

It was once thought that surges of the neurotransmitter dopamine produced by drugs directly caused the euphoria, but scientists now think dopamine has more to do with getting us to repeat pleasurable activities (reinforcement) than with producing pleasure directly.

Other Influences

Numerous other influences can affect the health of the immune system as well. In societies where smoking is acceptable, for example, people are more at risk for lung cancer and respiratory ailments, both of which can lead to various secondary infections, including bronchitis. Second-hand smoke, or passive smoking, increases respiratory infections for both infants and children. Children who are exposed to second-hand smoke may be predisposed to pneumonia, allergies * , and asthma * as well as repeated irritations of the eyes, nose, and mouth.

Nutrition, too, has an impact on the immune system. Malnutrition, with diets deficient in a variety of nutrients, such as certain vitamins, minerals, or protein, can cause increased vulnerability to infection.

* liver is a large organ located beneath the ribs on the right side of the body. The liver performs numerous digestive and chemical functions essential for health.

* allergies are immune system-related sensitivities to certain substances, for example, cat dander or the pollen of certain plants, that cause various reactions, such as sneezing, runny nose, wheezing, or swollen, itchy patches on the skin, called hives.

* asthma (AZ-mah) is a condition in which the airways of the lungs repeatedly become narrowed and inflamed, causing breathing difficulty.

Students will create an 8- page booklet to help them learn and review cell structures. The activities in the booklet will include the following:

A cut and paste activity to match the structure and function to the cell name

Label the structures of a plant cell diagram

Label the structures of an animal cell diagram

Review structures and functions by completing a crossword puzzle

Complete a Venn diagram showing differences/similarities of plant and animal cells.

Create a drawing of a cancer cell with unusual features.

History of 5-ALA industrialization

Since the discovery of 5-ALA by the late Dr. David Shemin (Columbia University, U.S.A.) in the 1950s [3] , many scientists worked on its basic biology throughout the 20th century. However, chemically synthesizing the 5-ALA used in basic research proved to be extremely complicated, and was more expensive than platinum by weight.

However, as the potential for the medical applications of 5-ALA became evident in the late 20th century, efforts to mass produce 5-ALA increased. Hiroshima University and Cosmo Oil's research team focused on the vigorous 5-ALA-producing ability of Rhodobacter sphaeroides, a photosynthetic microorganism commonly found in rice fields. From the many types of Rhodobacter sphaeroides, the best were repeatedly selected and propagated from countless individual specimens.

Through generations of selection, a strain that had both high 5-ALA production capacity and non-light-requiring properties, and that could be conveniently mass produced and successfully manufactured at the industrial level, was finally realized.

This microbial fermentation method can be widely adopted by anyone as it does not use genetic recombination , and we took over research. Now 5-ALA produced by this method is used in all the pharmaceuticals, health foods and other products produced by SBI Pharmaceuticals.

We continuously work with our partner companies and research institutes to further develop our products and improve our manufacturing technology to ensure that 5-ALA-based products reach more people.

Currently, 5-ALA products made by our company include 5-ALA hydrochloride, used in pharmaceutical products, and 5-ALA phosphate, used in health foods, cosmetics, and animal feed. 5-ALA phosphate used in foods has been registered as an ingredient that can be used as food in the Drug/non-drug list specified by the Ministry of Health, Labour and Welfare (MHLW) of Japan. Our 5-ALA has passed the quality control standards set by the MHLW based on applicable laws. Both pharmaceuticals and health foods have been manufactured to meet the manufacturing standards known as “Good Manufacturing Practice (GMP)” for medicine and “GMP for Dietary Supplements”. Our pharmaceuticals have been available since 2013 and our health foods since 2010.

How does ingested 5-ALA become heme?

In many cases, simply ingesting a substance that originally exists in the living body will not reach its place of origin or the place where its effects are needed. Just as a car cannot move by spraying gasoline over the rear seats, biological substances cannot function unless supplied in the correct manner.

However, for 5-ALA, there are two “coincidences” that enable its oral ingestion to exert its original function and change into heme.

The first “coincidence” is that 5-ALA produced in our body is assembled into heme in an unusual way. 5-ALA is created in mitochondria, tiny organs (organelles) inside the cell, but is immediately expelled from the mitochondria . After being assembled almost into its final form outside the mitochondria, it is then reintroduced into the mitochondria , and in the final step it bonds with iron (iron atoms) to complete the heme production (upper figure).It is not clear why such a seemingly inefficient process is employed, but it could be related to the fact that mitochondria once were “parasitic” organisms for us billions of years ago. As they lost their ability to live alone in the course of evolution, they transformed into organelles within us [4]. Because our ancestors adopted some of the mitochondria’s heme-producing ability to exploit this enormous energy-producing organism, the middle process of heme assembly may have taken place in “our side,” or outside mitochondria.

The second “coincidence” is the size of 5-ALA . In general, water-soluble substances like 5-ALA cannot pass through cells, but 5-ALA’s structure and size is similar to dipeptide, a two-amino-acid chain produced during the breakdown of protein (food) , and can pass through cells using a gate (called transporter) for dipeptides on the cell surface [5].

Due to these two “coincidences,” 5-ALA orally ingested and 5-ALA produced in the body are combined inside the cell/outside the mitochondria and together form heme.

Are these “coincidences” actually a coincidence or are they inevitable? In other words, was this trait for some reason essential in the evolutionary survival race of organisms? Only Mother Nature knows.

Regardless, we are designed to enjoy the blessings of 5-ALA by oral ingestion.

In many cases, simply ingesting a substance that originally exists in the living body will not reach its place of origin or the place where its effects are needed. Just as a car cannot move by spraying gasoline over the rear seats, biological substances cannot function unless supplied in the correct manner.

However, for 5-ALA, there are two “coincidences” that enable its oral ingestion to exert its original function and change into heme.

The first “coincidence” is that 5-ALA produced in our body is assembled into heme in an unusual way. 5-ALA is created in mitochondria, tiny organs (organelles) inside the cell, but is immediately expelled from the mitochondria . After being assembled almost into its final form outside the mitochondria, it is then reintroduced into the mitochondria , and in the final step it bonds with iron (iron atoms) to complete the heme production (upper figure).It is not clear why such a seemingly inefficient process is employed, but it could be related to the fact that mitochondria once were “parasitic” organisms for us billions of years ago. As they lost their ability to live alone in the course of evolution, they transformed into organelles within us [4]. Because our ancestors adopted some of the mitochondria’s heme-producing ability to exploit this enormous energy-producing organism, the middle process of heme assembly may have taken place in “our side,” or outside mitochondria.

The second “coincidence” is the size of 5-ALA . In general, water-soluble substances like 5-ALA cannot pass through cells, but 5-ALA’s structure and size is similar to dipeptide, a two-amino-acid chain produced during the breakdown of protein (food) , and can pass through cells using a gate (called transporter) for dipeptides on the cell surface [5].

Due to these two “coincidences,” 5-ALA orally ingested and 5-ALA produced in the body are combined inside the cell/outside the mitochondria and together form heme.

Are these “coincidences” actually a coincidence or are they inevitable? In other words, was this trait for some reason essential in the evolutionary survival race of organisms? Only Mother Nature knows.

Regardless, we are designed to enjoy the blessings of 5-ALA by oral ingestion.

Practice Questions

Review Questions

1. Because they are embedded within the membrane, ion channels are examples of ________.

  1. receptor proteins
  2. integral proteins
  3. peripheral proteins
  4. glycoproteins

2. The diffusion of substances within a solution tends to move those substances ________ their ________ gradient.

3. Ion pumps and phagocytosis are both examples of ________.

  1. endocytosis
  2. passive transport
  3. active transport
  4. facilitated diffusion

4. Choose the answer that best completes the following analogy: Diffusion is to ________ as endocytosis is to ________.

  1. filtration phagocytosis
  2. osmosis pinocytosis
  3. solutes fluid
  4. gradient chemical energy

Critical Thinking Questions

1. What materials can easily diffuse through the lipid bilayer, and why?

2. Why is receptor-mediated endocytosis said to be more selective than phagocytosis or pinocytosis?

3. What do osmosis, diffusion, filtration, and the movement of ions away from like charge all have in common? In what way do they differ?

Key Takeaway

  • Solution concentrations are typically expressed as molarity and can be prepared by dissolving a known mass of solute in a solvent or diluting a stock solution.

Conceptual Problems

Which of the representations best corresponds to a 1 M aqueous solution of each compound? Justify your answers.

Which of the representations shown in Problem 1 best corresponds to a 1 M aqueous solution of each compound? Justify your answers.

Would you expect a 1.0 M solution of CaCl2 to be a better conductor of electricity than a 1.0 M solution of NaCl? Why or why not?

An alternative way to define the concentration of a solution is molality, abbreviated m. Molality is defined as the number of moles of solute in 1 kg of solvent. How is this different from molarity? Would you expect a 1 M solution of sucrose to be more or less concentrated than a 1 m solution of sucrose? Explain your answer.

What are the advantages of using solutions for quantitative calculations?


If the amount of a substance required for a reaction is too small to be weighed accurately, the use of a solution of the substance, in which the solute is dispersed in a much larger mass of solvent, allows chemists to measure the quantity of the substance more accurately.

Numerical Problems

Calculate the number of grams of solute in 1.000 L of each solution.

  1. 0.2593 M NaBrO3
  2. 1.592 M KNO3
  3. 1.559 M acetic acid
  4. 0.943 M potassium iodate

Calculate the number of grams of solute in 1.000 L of each solution.

If all solutions contain the same solute, which solution contains the greater mass of solute?

  1. 1.40 L of a 0.334 M solution or 1.10 L of a 0.420 M solution
  2. 25.0 mL of a 0.134 M solution or 10.0 mL of a 0.295 M solution
  3. 250 mL of a 0.489 M solution or 150 mL of a 0.769 M solution

Complete the following table for 500 mL of solution.

Compound Mass (g) Moles Concentration (M)
calcium sulfate 4.86
acetic acid 3.62
hydrogen iodide dihydrate 1.273
barium bromide 3.92
glucose 0.983
sodium acetate 2.42

What is the concentration of each species present in the following aqueous solutions?

  1. 0.489 mol of NiSO4 in 600 mL of solution
  2. 1.045 mol of magnesium bromide in 500 mL of solution
  3. 0.146 mol of glucose in 800 mL of solution
  4. 0.479 mol of CeCl3 in 700 mL of solution

What is the concentration of each species present in the following aqueous solutions?

  1. 0.324 mol of K2MoO4 in 250 mL of solution
  2. 0.528 mol of potassium formate in 300 mL of solution
  3. 0.477 mol of KClO3 in 900 mL of solution
  4. 0.378 mol of potassium iodide in 750 mL of solution

What is the molar concentration of each solution?

  1. 8.7 g of calcium bromide in 250 mL of solution
  2. 9.8 g of lithium sulfate in 300 mL of solution
  3. 12.4 g of sucrose (C12H22O11) in 750 mL of solution
  4. 14.2 g of iron(III) nitrate hexahydrate in 300 mL of solution

What is the molar concentration of each solution?

  1. 12.8 g of sodium hydrogen sulfate in 400 mL of solution
  2. 7.5 g of potassium hydrogen phosphate in 250 mL of solution
  3. 11.4 g of barium chloride in 350 mL of solution
  4. 4.3 g of tartaric acid (C4H6O6) in 250 mL of solution

Give the concentration of each reactant in the following equations, assuming 20.0 g of each and a solution volume of 250 mL for each reactant.

  1. BaCl2(aq) + Na2SO4(aq) →
  2. Ca(OH)2(aq) + H3PO4(aq) →
  3. Al(NO3)3(aq) + H2SO4(aq) →
  4. Pb(NO3)2(aq) + CuSO4(aq) →
  5. Al(CH3CO2)3(aq) + NaOH(aq) →

An experiment required 200.0 mL of a 0.330 M solution of Na2CrO4. A stock solution of Na2CrO4 containing 20.0% solute by mass with a density of 1.19 g/cm 3 was used to prepare this solution. Describe how to prepare 200.0 mL of a 0.330 M solution of Na2CrO4 using the stock solution.

Calcium hypochlorite [Ca(OCl)2] is an effective disinfectant for clothing and bedding. If a solution has a Ca(OCl)2 concentration of 3.4 g per 100 mL of solution, what is the molarity of hypochlorite?

Phenol (C6H5OH) is often used as an antiseptic in mouthwashes and throat lozenges. If a mouthwash has a phenol concentration of 1.5 g per 100 mL of solution, what is the molarity of phenol?

If a tablet containing 100 mg of caffeine (C8H10N4O2) is dissolved in water to give 10.0 oz of solution, what is the molar concentration of caffeine in the solution?

A certain drug label carries instructions to add 10.0 mL of sterile water, stating that each milliliter of the resulting solution will contain 0.500 g of medication. If a patient has a prescribed dose of 900.0 mg, how many milliliters of the solution should be administered?

In biology, poisons are substances that can cause death, injury or harm to organs, tissues, cells, and DNA usually by chemical reactions or other activity on the molecular scales, when an organism is exposed to a sufficient quantity.

Iron poisoning typically occurs from ingestion of excess iron that results in acute toxicity. Mild symptoms which occur within hours include vomiting, diarrhea, abdominal pain, and drowsiness. In more severe cases, symptoms can include tachypnea, low blood pressure, seizures, or coma. If left untreated, iron poisoning can lead to multi-organ failure resulting in permanent organ damage or death.

Lead poisoning, also known as plumbism and saturnism, is a type of metal poisoning caused by lead in the body. The brain is the most sensitive. Symptoms may include abdominal pain, constipation, headaches, irritability, memory problems, infertility, and tingling in the hands and feet. It causes almost 10% of intellectual disability of otherwise unknown cause and can result in behavioral problems. Some of the effects are permanent. In severe cases, anemia, seizures, coma, or death may occur.

Detoxification or detoxication is the physiological or medicinal removal of toxic substances from a living organism, including the human body, which is mainly carried out by the liver. Additionally, it can refer to the period of drug withdrawal during which an organism returns to homeostasis after long-term use of an addictive substance. In medicine, detoxification can be achieved by decontamination of poison ingestion and the use of antidotes as well as techniques such as dialysis and chelation therapy.

A pesticide poisoning occurs when pesticides, chemicals intended to control a pest, affect non-target organisms such as humans, wildlife, plant, or bees. There are three types of pesticide poisoning. The first of the three is a single and short-term very high level of exposure which can be experienced by individuals who commit suicide, as well as pesticide formulators. The second type of poisoning is long-term high-level exposure, which can occur in pesticide formulators and manufacturers. The third type of poisoning is a long-term low-level exposure, which individuals are exposed to from sources such as pesticide residues in food as well as contact with pesticide residues in the air, water, soil, sediment, food materials, plants and animals.

Chlorfenvinphos is the common name of an organophosphorus compound that was widely used as an insecticide and an acaricide. The molecule itself can be described as an enol ester derived from dichloroacetophenone and diethylphosphonic acid. Chlorfenvinphos has been included in many products since its first use in 1963. However, because of its toxic effect as a cholinesterase inhibitor it has been banned in several countries, including the United States and the European Union. Its use in the United States was cancelled in 1991.

Ethion (C9H22O4P2S4) is an organophosphate insecticide. Ethion is known to affect a neural enzyme called acetylcholinesterase and prevent it from working.

Cadmium is a naturally occurring toxic metal with common exposure in industrial workplaces, plant soils, and from smoking. Due to its low permissible exposure in humans, overexposure may occur even in situations where trace quantities of cadmium are found. Cadmium is used extensively in electroplating, although the nature of the operation does not generally lead to overexposure. Cadmium is also found in some industrial paints and may represent a hazard when sprayed. Operations involving removal of cadmium paints by scraping or blasting may pose a significant hazard. The primary use of cadmium is in the manufacturing of NiCd rechargeable batteries. The primary source for cadmium is as a byproduct of refining zinc metal. Exposures to cadmium are addressed in specific standards for the general industry, shipyard employment, the construction industry, and the agricultural industry.

Abrin is an extremely toxic toxalbumin found in the seeds of the rosary pea, Abrus precatorius. It has a median toxic dose of 0.7 micrograms per kilogram of body mass when given to mice intravenously. The median toxic dose for humans ranges from 10 to 1000 micrograms per kilogram when ingested and is 3.3 micrograms per kilogram when inhaled.

Endrin is an organochloride with the chemical formula C12H8Cl6O that was first produced in 1950 by Shell and Velsicol Chemical Corporation. It was primarily used as an insecticide, as well as a rodenticide and piscicide. It is a colourless, odorless solid, although commercial samples are often off-white. Endrin was manufactured as an emulsifiable solution known commercially as Endrex. The compound became infamous as a persistent organic pollutant and for this reason it is banned in many countries.

Phosmet is a phthalimide-derived, non-systemic, organophosphate insecticide used on plants and animals. It is mainly used on apple trees for control of codling moth, though it is also used on a wide range of fruit crops, ornamentals, and vines for the control of aphids, suckers, mites, and fruit flies.

Organophosphate poisoning is poisoning due to organophosphates (OPs). Organophosphates are used as insecticides, medications, and nerve agents. Symptoms include increased saliva and tear production, diarrhea, vomiting, small pupils, sweating, muscle tremors, and confusion. While onset of symptoms is often within minutes to hours, some symptoms can take weeks to appear. Symptoms can last for days to weeks.

Metal toxicity or metal poisoning is the toxic effect of certain metals in certain forms and doses on life. Some metals are toxic when they form poisonous soluble compounds. Certain metals have no biological role, i.e. are not essential minerals, or are toxic when in a certain form. In the case of lead, any measurable amount may have negative health effects. Often heavy metals are thought as synonymous, but lighter metals may also be toxic in certain circumstances, such as beryllium and lithium. Not all heavy metals are particularly toxic, and some are essential, such as iron. The definition may also include trace elements when in abnormally high doses may be toxic. An option for treatment of metal poisoning may be chelation therapy, which is a technique which involves the administration of chelation agents to remove metals from the body.

Ethylene glycol poisoning is poisoning caused by drinking ethylene glycol. Early symptoms include intoxication, vomiting and abdominal pain. Later symptoms may include a decreased level of consciousness, headache, and seizures. Long term outcomes may include kidney failure and brain damage. Toxicity and death may occur after drinking even a small amount.

Paracetamol poisoning, also known as acetaminophen poisoning, is caused by excessive use of the medication paracetamol (acetaminophen). Most people have few or non-specific symptoms in the first 24 hours following overdose. These include feeling tired, abdominal pain, or nausea. This is typically followed by a couple of days without any symptoms, after which yellowish skin, blood clotting problems, and confusion occurs as a result of liver failure. Additional complications may include kidney failure, pancreatitis, low blood sugar, and lactic acidosis. If death does not occur, people tend to recover fully over a couple of weeks. Without treatment, death from toxicity occurs 4 to 18 days later.

Chlorethoxyfos is an organophosphate acetylcholinesterase inhibitor used as an insecticide. It is registered for the control of corn rootworms, wireworms, cutworms, seed corn maggot, white grubs and symphylans on corn. The insecticide is sold under the trade name Fortress by E.I. du Pont de Nemours & Company.

Salicylate poisoning, also known as aspirin poisoning, is the acute or chronic poisoning with a salicylate such as aspirin. The classic symptoms are ringing in the ears, nausea, abdominal pain, and a fast breathing rate. Early on, these may be subtle, while larger doses may result in fever. Complications can include swelling of the brain or lungs, seizures, low blood sugar, or cardiac arrest.

Pyrrolizidine alkaloidosis is a disease caused by chronic poisoning found in humans and other animals caused by ingesting poisonous plants which contain the natural chemical compounds known as pyrrolizidine alkaloids. Pyrrolizidine alkaloidosis can result in damage to the liver, kidneys, heart, brain, smooth muscles, lungs, DNA, lesions all over the body, and could be a potential cause of cancer. Pyrrolizidine alkaloidosis is known by many other names such as "Pictou Disease" in Canada and "Winton Disease" in New Zealand. Cereal crops and forage crops can sometimes become polluted with pyrrolizidine-containing seeds, resulting in the alkaloids contaminating flour and other foods, including milk from cows feeding on these plants.

Terbufos is a chemical compound used in insecticides and nematicides. Terbufos is part of the chemical family of organophosphates. It is a clear, colourless to pale yellow or reddish-brown liquid and sold commercially as granulate.

Methanol toxicity is poisoning from methanol, characteristically via ingestion. Symptoms may include a decreased level of consciousness, poor or no coordination, vomiting, abdominal pain, and a specific smell on the breath. Decreased vision may start as early as twelve hours after exposure. Long-term outcomes may include blindness and kidney failure. Toxicity and death may occur even after drinking a small amount.


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