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α-Amanitin is a bicyclic peptide which belongs to a large group ..
α-Amanitin acts in vitro as a selective inhibitor of the nucleoplasmic form B RNA polymerases. Treatment of Chinese hamster ovary (CHO) cells with this drug leads principally to a severe fragmentation of the nucleoli. While the ultrastructural lesions induced by α-amanitin in CHO cells and in rat or mouse liver are quite similar, the results diverge concerning the effect on RNA synthesis. It has been shown that in rat or mouse liver α-amanitin blocks both extranucleolar and nucleolar RNA synthesis. Our autoradiographic and biochemical evidence indicates that in CHO cells high molecular weight extranucleolar RNA synthesis (HnRNA) is blocked by the α-amanitin treatment, whereas nucleolar RNA (preribosomal RNA) synthesis remains unaffected even several hours after the inhibition of extranucleolar RNA synthesis. Furthermore, the processing of this RNA as well as its transport to the cytoplasm seem only slightly affected by the treatment. Finally, under these conditions, the synthesis of the low molecular RNA species (4–5S) still occurs, though less actively. The results are interpreted as evidence for a selective impairment of HnRNA synthesis by α-amanitin in CHO cells.
AB - Influenza virus polypeptides were not synthesized in wild-type CHO-S-infected cells in the presence of α-amanitin, but were synthesized in CHO-Ama1 cells, a mutant cell line whose DNA-dependent RNA polymerase II is specifically resistant to this drug, indicating that this cellular enzyme is involved in influenza virus replication. The results of experiments designed to detect viral polypeptides synthesized from primary transcripts suggest that the synthesis of a cellular RNA species by RNA polymerase II is required for primary transcription of the influenza virus genome.
Thermostability of alpha amanitin in water and …
Subsequent events may be divided into four stages. (1) A latent period of 6-24 hours, most commonly about 12 hours. This asymptomatic interlude is long enough that the patient frequently does not even connect the subsequent illness with mushrooms. During this hiatus,the amanitin is attacking the cells of the liver, kidney and intestine. (2) Violent vomiting, diarrhea and abdominal pain, which last for a day or so. (3) A brief, misleading remission of symptoms. (4) Collapse of kidney and liver function, with secondary effects on the heart and brain, leading to coma and death.
As a fascinating biological footnote, I must mention that several mycophagous species of Drosophila (the fruit fly genus) eat poisonous amanitas with impunity. It has been demonstrated that they can survive concentrations of amanitin hundreds of times greater than can their fruit-feeding relatives. They are, in fact, the most amanitin-tolerant species known. Although we do not know exactly how they deal with the toxin, we now know two things which may have driven the evolution of this tolerance. First, although the agarics in which mycophagous drosophilas breed are also sought out by crane flies and wood gnats, much larger insects, those competitors cannot survive in mushrooms that contain amanitin. Second, Drosophila larvae in amanitin-containing mushrooms are never parasitized by the nematode, Howardula. This is an important selective advantage, because parasitized adults, which can represent up to 35% of the population, are often sterile or have reduced breeding success. There is an old saying: "It's an ill wind that blows nobody any good." It certainly seems that the presence of amanitin in some agarics is a real boon to Drosophila, if not to people.
Alpha-Amanitin: Background and Mechanism - YouTube
(1) Toxins that cause extensive cell destruction, but which produce overt symptoms only after a significant, and potentially fatal, delay (amanitin, orellanine, monomethylhydrazine).
The seven kinds of poisoning already described are now fairly well understood. Most of the relatively few fungi involved are clearly identified as containing specific toxins which cause well-defined sets of symptoms. In contrast, the seventh kind of poisoning is caused by a grab-bag of fleshy fungi belonging to many different genera. They have only one thing in common: within 30-90 minutes of being eaten, all cause various degrees of digestive upset. The commonest symptoms are vomiting and diarrhea, with abdominal cramps. Fortunately, the similarity to amanitin poisoning ends there. Symptoms generally clear up spontaneously in 3-4 hours, and complete recovery takes only a day or so.
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amanitin - University of Wisconsin–Eau Claire
Since most North Americans are kickers, they tend not to become mushroom poisoning statistics. Europeans, however, are pickers, and have suffered as many as 100 fatalities in two weeks. In 1975, a Swiss newspaper reported 54 local deaths during a short period in late summer. Which fungi killed these people? What are the toxins involved? We recognize eight different kinds of mushroom poisoning, which are listed in the. A quick look at this table will show that fatalities are usually caused only by groups I, II and III. In fact, 50% of all serious mushroom poisonings, and 95% of all fatalities, are caused by members of a single genus, Amanita, which fruits in late summer and fall.
of amanitin directly affects the ..
Influenza virus polypeptides were not synthesized in wild-type CHO-S-infected cells in the presence of α-amanitin, but were synthesized in CHO-Ama1 cells, a mutant cell line whose DNA-dependent RNA polymerase II is specifically resistant to this drug, indicating that this cellular enzyme is involved in influenza virus replication. The results of experiments designed to detect viral polypeptides synthesized from primary transcripts suggest that the synthesis of a cellular RNA species by RNA polymerase II is required for primary transcription of the influenza virus genome.
Death cap mushrooms produce a substance called alpha-amanitin
N2 - Influenza virus polypeptides were not synthesized in wild-type CHO-S-infected cells in the presence of α-amanitin, but were synthesized in CHO-Ama1 cells, a mutant cell line whose DNA-dependent RNA polymerase II is specifically resistant to this drug, indicating that this cellular enzyme is involved in influenza virus replication. The results of experiments designed to detect viral polypeptides synthesized from primary transcripts suggest that the synthesis of a cellular RNA species by RNA polymerase II is required for primary transcription of the influenza virus genome.
alpha-Amanitin, Amanita sp. - supplier and …
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