Emily Johnson
Death cap mushrooms, or Amanita phalloides, are one of the most poisonous mushrooms in the world, causing 90% of mushroom poisoning deaths worldwide. The toxins in death cap mushrooms primarily target the liver, but other organs, such as the kidneys, are also affected. Amatoxins, the main toxin in death cap mushrooms, prevent the production of DNA and stop protein synthesis in cells, causing cell death. Other toxins found in death cap mushrooms include phallotoxins and virotoxins. While there is currently no definitive antidote for death cap mushroom poisoning, treatments such as high-dose intravenous penicillin G and intravenous silibinin have been shown to improve survivability.
| Characteristics | Values |
|---|---|
| Common name | Death Cap |
| Scientific name | Amanita phalloides |
| Type | Basidiomycete fungus and mushroom |
| Toxins | Amatoxins, Phallotoxins, Virotoxins |
| Most toxic toxin | ɑ-Amanitin |
| Toxin effect | Stops cells from making proteins |
| Organs affected | Liver, Kidneys |
| Symptoms | Nausea, Vomiting, Jaundice, Seizures, Coma |
| Treatment | Silibinin, Liver Transplant |
| Preventative measures | Do not touch, avoid putting with edible fungi |
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What You'll Learn
Amatoxins prevent DNA production
Death cap mushrooms, or Amanita phalloides, are highly toxic and responsible for the majority of fatal mushroom poisonings worldwide. The toxins in death cap mushrooms primarily target the liver, but other organs, such as the kidneys, are also affected. Amatoxins, one of the three main groups of toxins found in death cap mushrooms, prevent the production of DNA, leading to liver and kidney failure, and, if untreated, coma and death.
Amatoxins are a type of alkaloid, a naturally occurring chemical. Alkaloids are typically found in organic matter like plants and fungi. Amatoxins are extremely dangerous and can stop protein synthesis in cells, causing cell death. The RNA polymerase of Amanita phalloides is insensitive to the effects of amatoxins, so the mushroom does not poison itself. However, when consumed by humans, amatoxins inhibit an enzyme called RNA polymerase II, preventing cells from carrying out essential functions such as creating proteins.
The toxin has the same effect on all the cells it interacts with, and within one to seven days of ingestion, the death cap can result in liver failure, kidney failure, encephalopathy, and death. The binding of amatoxins to cells is largely irreversible, making it challenging to find an effective antidote. The quicker the treatment is administered, the better the prognosis.
Some treatments that have shown to improve survivability include high-dose continuous intravenous penicillin G and intravenous silibinin, an extract from the blessed milk thistle (Silybum marianum). Silibinin prevents the uptake of amatoxins by liver cells, thereby protecting undamaged liver tissue. It also stimulates DNA-dependent RNA polymerases, leading to an increase in RNA synthesis.
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Amatoxins stop protein synthesis
Amatoxins are a type of alkaloid, a naturally occurring chemical. Amatoxins are cyclic peptides that are synthesized as 35-amino-acid proproteins, from which the final eight amino acids are cleaved by a prolyl oligopeptidase. They are a group of toxins found in death cap mushrooms, also known by their scientific name Amanita phalloides. Amatoxins are the most toxic of the three broad classes of toxins found in death caps, the other two being phallotoxins and virotoxins.
Death cap mushrooms are highly toxic and responsible for the majority of fatal mushroom poisonings worldwide. Amatoxins are potent and selective inhibitors of RNA polymerase II (RNA Pol II), a vital enzyme in the synthesis of messenger RNA (mRNA), microRNA, and small nuclear RNA (snRNA). Without mRNA, which is the template for protein synthesis, cell metabolism stops, and apoptosis ensues.
Amatoxins primarily affect the bridge helix of the RNA Pol II complex, a highly conserved domain 35 amino acids long. Amatoxins bind to the bridge helix of the RNA Pol II complex, locking the bridge helix into place and dramatically slowing its movement in translocating DNA. This inhibition of RNA polymerase II in cell nuclei and DNA transcription prevents protein synthesis, curtailing cell metabolism.
The liver is the principal organ affected by amatoxins, as it is the first organ encountered after absorption in the gastrointestinal tract. However, other organs, such as the kidneys, are also susceptible to damage. Amatoxins cause perforations in the plasma membranes of cells, resulting in misplaced organelles in the extracellular matrix. This damage to the liver and kidneys can lead to organ failure and death.
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Phallotoxins are toxic to liver cells
Death cap mushrooms, or Amanita phalloides, are highly toxic fungi responsible for the majority of fatal mushroom poisonings worldwide. They contain a high concentration of toxins, including amatoxins, phallotoxins, and virotoxins. While amatoxins are the most toxic of these compounds, phallotoxins are also highly toxic to liver cells.
Phallotoxins consist of at least seven compounds, all of which are bicyclic heptapeptides (seven amino acids). They are isolated from the death cap mushroom and differ from amatoxins by being one residue smaller in the final product and the precursor protein. Phalloidin, one of the phallotoxins, was first isolated in 1937 and is also found in the edible and sought-after blusher (Amanita rubescens) mushroom.
Although phallotoxins are highly toxic to liver cells, they have been found to contribute little to the overall toxicity of death cap mushrooms when ingested orally. This is because, unlike amatoxins, phallotoxins are not absorbed through the gut or from the gastrointestinal tract. Instead, they are toxic when given parenterally, meaning through a means other than the digestive tract.
The liver is the principal organ affected by death cap mushroom poisoning because it is the first organ encountered after absorption in the gastrointestinal tract. The toxins in death cap mushrooms can cause liver failure, and in severe cases, a liver transplant may be necessary.
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Virotoxins are another toxin in death caps
Death cap mushrooms, or Amanita phalloides, are deadly poisonous basidiomycete fungi and mushrooms. They are responsible for the majority of fatal mushroom poisonings worldwide. The toxins in death cap mushrooms primarily target the liver, but other organs, such as the kidneys, are also affected.
Death cap mushrooms contain three broad classes of toxins: amatoxins, phallotoxins, and virotoxins. Amatoxins are a type of alkaloid, a naturally occurring chemical, that can stop protein synthesis in cells, causing the cells to die. Phallotoxins are highly toxic to liver cells, but they are not absorbed through the gut and therefore add little to the death cap's toxicity.
Virotoxins are another toxin found in death cap mushrooms. They consist of six similar monocyclic heptapeptides. While the specific function of virotoxins is unknown, they are believed to play a role in the overall toxicity of death cap mushrooms. Virotoxins may work synergistically with other toxins or have unique effects on their own. The synergistic effects of multiple toxins working together could be one reason why death cap mushrooms are so deadly.
The specific mechanisms by which virotoxins contribute to the toxicity of death cap mushrooms are still being studied. However, it is clear that they play a role in making these mushrooms extremely dangerous to humans. The complex interplay of different toxins in death cap mushrooms underscores the importance of avoiding consumption and seeking immediate medical attention if accidental ingestion occurs.
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Treatments include liver transplant
Death cap mushrooms contain a high concentration of compounds called amatoxins, a type of alkaloid. Amatoxins are highly toxic and can stop protein synthesis in cells, causing them to die. The toxins primarily target the liver, but other organs, such as the kidneys, are also affected.
Treatments for death cap mushroom poisoning vary depending on the time since ingestion. It is critical to receive treatment early to prevent liver and kidney damage. Treatment in the early stages focuses on stabilizing the patient and counteracting the toxin's effects.
If a patient is in an advanced stage of poisoning, extreme measures like a liver transplant may be necessary. In cases of liver failure, if the patient is well enough, a liver transplant may be performed.
While there is currently no definitive antidote for death cap mushroom poisoning, some treatments have shown promising results in improving survivability. High-dose intravenous penicillin G has been reported to be beneficial, although the mechanism is not fully understood. Intravenous silibinin, a compound derived from the blessed milk thistle plant, has also shown potential in reducing the effects of poisoning by preventing the uptake of amatoxins by liver cells.
Additionally, indocyanine green (ICG), a medical imaging dye, has been identified as a potential antidote in mice, increasing the survival rate from 20% to 50%. However, it has not yet been tested in humans.
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Frequently asked questions
The death cap mushroom contains three broad classes of toxins: amatoxins, phallotoxins, and virotoxins.
Amatoxins inhibit an enzyme called RNA polymerase II, preventing cells from carrying out essential functions such as creating proteins. This causes the cells to die.
The first symptoms of death cap mushroom toxicity usually occur 6 to 12 hours after ingestion. These symptoms include nausea, vomiting, abdominal pain, and diarrhea. After 12 to 36 hours, the first wave of symptoms passes, and patients may feel better. However, during this stage, the toxins are still affecting the body and damaging the liver and kidneys. If left untreated, death cap mushroom poisoning can lead to liver and kidney failure, encephalopathy, coma, and death.
There is currently no definitive antidote for death-cap mushroom poisoning. However, some treatments have been shown to improve survivability, such as high-dose intravenous penicillin G and intravenous silibinin, an extract from the blessed milk thistle.
