Қауіпті саңырауқұлақ – Ақ зеңгеш (Amanita virosa)

Species of fungus

Amanita virosa is a species of fungus in the class Agaricomycetes. In the UK, it has the recommended English name of destroying angel and is known internationally as the European destroying angel. Basidiocarps (fruit bodies) are agaricoid (mushroom shaped) and pure white with an ring on the stem and a sack like volva at the base. The species is deadly poisonous. It occurs in Europe and northern Asia. Amanita virosa was formerly reported from North America, but research has shown that similar looking American species, including Amanita bisporigera and A. ocreata, are distinct.

Amanita virosa was first described in 1838 by Swedish mycologist Elias Magnus Fries as Agaricus virosus, but this name is illegitimate since it had already been used for an earlier and different species. Amanita virosa was legitimately published by French mycologist Louis Adolphe Bertillon in 1866.

The specific epithet is derived from the Latin adjective virōsus meaning 'toxic' (compare virus).

Amanita virosa first appears as a white, egg shaped object covered with a universal veil. As it expands, the mushroom shaped fruit body breaks free, though ragged patches of veil may persist at the cap edges. The cap is initially conical with inturned edges, before becoming hemispherical and flattening with a diameter up to The cap often has a distinctive boss; it is able to be peeled and is white, though the centre may be ivory. The crowded, free gills are white, as is the stipe and volva. The thin stipe is up to tall, with a hanging, grooved ring. The spore print is white and the spores are subglobose and 7–10 μm long. They are amyloid, staining purple with Melzer's reagent. The flesh is white, with a smell reminiscent of radishes, and turns bright yellow with sodium hydroxide.

In Europe, the spring fruiting Amanita verna is a similar all white species, as is the autumn fruiting, white form of Amanita phalloides (deathcap). Both are equally poisonous. In their immature, button mushroom stage, all these poisonous species could be mistaken for young, white capped, edible mushrooms (Agaricus species), highlighting the danger of picking immature fruit bodies for food.

Amanita virosa is found in woodland in late summer and autumn, especially in association with beech and chestnut, but also with pine, spruce, and fir. The symptoms of poisoning generally come several hours after consumption, a delay which may make treatment more difficult. Fruit bodies contain both amatoxins and phallotoxins. Amatoxins consist of at least eight compounds with a similar structure, that of eight amino acid rings; they were isolated in 1941 by Heinrich O. Wieland and Rudolf Hallermayer of the University of Munich. Of the amatoxins, α Amanitin is the chief component and along with β Amanitin is probably responsible for the toxic effects. Their major toxic mechanism is the inhibition of RNA polymerase II, a vital enzyme in the synthesis of messenger RNA (mRNA), microRNA, and small nuclear RNA, (snRNA). Without mRNA essential protein synthesis and hence cell metabolism cease and the cell dies. The liver is the principal organ affected, as it is the organ which is first encountered after absorption in the gastrointestinal tract, though other organs, especially the kidneys, are susceptible. they have since been found to have little input into the destroying angel's toxicity as they are not absorbed through the gut. Like the phallotoxins they do not exert any acute toxicity after ingestion in humans. Some authorities strongly advise against putting fruit bodies in the same basket with those collected for the table and to avoid handling them.

Consumption of Amanita virosa is a medical emergency requiring hospitalization. There are four main categories of therapy for poisoning: preliminary medical care, supportive measures, specific treatments, and liver transplantation. Preliminary care consists of gastric decontamination with either activated carbon or gastric lavage. However, due to the delay between ingestion and the first symptoms of poisoning, it is commonplace for patients to arrive for treatment many hours after ingestion, potentially reducing the efficacy of these interventions. Supportive measures are directed towards treating the dehydration which results from fluid loss during the gastrointestinal phase of intoxication and correction of metabolic acidosis, hypoglycemia, electrolyte imbalances, and impaired coagulation. and trials with cephalosporins show promise. There is some evidence that intravenous silibinin, an extract from the blessed milk thistle (Silybum marianum), may be beneficial in reducing the effects of death cap poisoning. Silibinin prevents the uptake of amatoxins by hepatocytes, thereby protecting undamaged hepatic tissue; it also stimulates DNA dependent RNA polymerases, leading to an increase in RNA synthesis. N acetylcysteine has shown promise in combination with other therapies. Animal studies indicate the amatoxins deplete hepatic glutathione; N acetylcysteine serves as a glutathione precursor and may therefore prevent reduced glutathione levels and subsequent liver damage. None of the antidotes used have undergone prospective, randomized clinical trials, and only anecdotal support is available. Silibinin and N acetylcysteine appear to be the therapies with the most potential benefit. Other methods of enhancing the elimination of the toxins have been trialed; techniques such as hemodialysis, hemoperfusion, plasmapheresis, and peritoneal dialysis have occasionally yielded success but overall do not appear to improve outcome. This is a complicated issue, however, as transplants themselves may have significant complications and mortality; patients require long term immunosuppression to maintain the transplant. Evidence suggests that, although survival rates have improved with modern medical treatment, in patients with moderate to severe poisoning up to half of those who did recover suffered permanent liver damage.

Amanita virosa extract has antibacterial efficacy against Pseudomonas aeruginosa and Staphylococcus aureus in vitro. It also has shown inhibitory activity on thrombin.