The toxic peptides from Amanita mushrooms

Wieland, Theodor

doi:10.1111/j.1399-3011.1983.tb02093.x

Cited by 143 publications

(68 citation statements)

References 106 publications

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“…To demonstrate the requirement for RNA-and proteindependent mechanisms in the cardioprotection afforded by CP, we used AMN, an irreversible inhibitor of nuclear and mitochondrial RNA transcription that acts by binding to RNA polymerase II, and CHX, an irreversible protein synthesis inhibitor that halts mRNA translation by blocking the translocation of tRNA at the ribosome (16,18,45). Our results showed that the inhibition of RNA or protein synthesis decreases the cardioprotection provided by CP (Table 2).…”

Section: Resultsmentioning

confidence: 99%

“…Control hearts (control ϩ AMN and control ϩ CHX) were then perfused for 155 min. CP hearts (CP ϩ AMN and CP ϩ CHX) received CP for 5 min before 30 min of GI and 120 min of reperfusion (16,18,45). Control hearts were preperfused for 55 min with Krebs-Ringer solution containing either AMN or CHX and then were perfused for 150 min with Krebs-Ringer solution alone (n ϭ 4 each).…”

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confidence: 99%

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Transcriptomic and proteomic analysis of global ischemia and cardioprotection in the rabbit heart

McCully

Bhasin

Daly

et al. 2009

Physiological Genomics

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scriptomic and proteomic analysis of global ischemia and cardioprotection in the rabbit heart. Physiol Genomics 38: 125-137, 2009. First published May 19, 2009 doi:10.1152/physiolgenomics.00033.2009Cardioplegia is used to partially alleviate the effects of surgically induced global ischemia injury; however, the molecular mechanisms involved in this cardioprotection remain to be elucidated. To improve the understanding of the molecular processes modulating the effects of global ischemia and the cardioprotection afforded by cardioplegia, we constructed rabbit heart cDNA libraries and isolated, sequenced, and identified a compendium of nonredundant cDNAs for use in transcriptomic and proteomic analyses. New Zealand White rabbits were used to compare the effects of global ischemia and cardioplegia compared with control (nonischemic) hearts. The effects of RNA and protein synthesis on the cardioprotection afforded by cardioplegia were investigated separately by preperfusion with either ␣-amanitin or cycloheximide. Our results demonstrate that cardioplegia partially ameliorates the effects of global ischemia and that the cardioprotection is modulated by RNA-and protein-dependent mechanisms. Transcriptomic and proteomic enrichment analyses indicated that global ischemia downregulated genes/proteins associated with mitochondrial function and energy production, cofactor catabolism, and the generation of precursor metabolites of energy. In contrast, cardioplegia significantly increased differentially expressed genes/proteins associated with the mitochondrion and mitochondrial function and significantly upregulated the biological processes of muscle contraction, involuntary muscle contraction, carboxylic acid and fatty acid catabolic processes, fatty acid ␤-oxidation, and fatty acid metabolic processes. mitochondrion; ischemia-reperfusion MYOCARDIAL ISCHEMIA-REPERFUSION INJURY occurs as the result of the attenuation or cessation of coronary blood flow such that oxygen delivery to the myocardium is insufficient to meet energy demands. The cessation of myocardial coronary blood flow induces a cascade of cellular events that rapidly alter myocardial cellular homeostasis, leading to cellular dysfunction and/or death and postischemic functional impairment (23).To alleviate the effects of surgically induced ischemia/ reperfusion injury, surgeons use cardioplegia (CP) solutions that allow for the rapid electromechanical arrest of the myocardium through the alteration of cellular electrochemical gradients (40). In a series of studies, we have shown that magnesium-supplemented potassium CP with the addition of diazoxide significantly decreases myocardial cell death and significantly enhances postischemic functional recovery (22,40,43).The mechanisms through which CP affords cardioprotection are complex and cannot be investigated as a single entity; rather, they must be investigated as a system. In previous reports, we and others have used a variety of methods to identify the RNAs and proteins associated with global ischemia (GI) a...

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Section: Resultsmentioning

confidence: 99%

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confidence: 99%

Transcriptomic and proteomic analysis of global ischemia and cardioprotection in the rabbit heart

McCully

Bhasin

Daly

et al. 2009

Physiological Genomics

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“…5 The pathological findings reflect the mechanism of action of amanitin, which binds to RNA polymerase II, inhibiting transcription of mRNA and leading to diminished protein synthesis and eventual cell death. 10,11 In reported cases, hepatocytes and renal proximal tubules are consistently affected, which may reflect high rates of protein synthesis in these cells. 4,6,7 Accordingly, serum chemistry values in cases of amanitin toxicosis reflect aberrations in hepatic, and often renal, function.…”

Section: Discussionmentioning

confidence: 99%

Amanitin Toxicosis in Two Cats with Acute Hepatic and Renal Failure

Tokarz

Poppenga²,

Kaae³

et al. 2011

Vet Pathol

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Amanitin is a toxic cyclopeptide present in several species of poisonous mushrooms. Amanitin toxicosis was diagnosed in 2 cats from separate premises. Both cats initially had lethargy and vomiting, and they rapidly developed depression and neurological signs over 24-48 hours. Marked elevation of alanine aminotransferase was the primary finding, with subsequent serum chemistry values compatible with hepatic and renal failure. Histopathological findings consisted of submassive to massive acute hepatic necrosis, renal proximal tubular epithelial necrosis, and foci of necrosis and inflammation in the gastrointestinal tract. Amanitin exposure was confirmed postmortem by detection of a-amanitin in the kidney by liquid chromatography-mass spectrometry. A similar clinical course and pathological changes are reported in human and canine amanitin intoxication; however, gastrointestinal lesions are not typically described. Keywords amanitins, cats, gastrointestinal tract, kidney, liver, mushroom poisoningAmanitins are cyclopeptides present in several species of poisonous mushrooms in the genera Amanita, Galerina, and Lepiota and are considered to be responsible for the potent toxicity of these mushroom species.5,10,11 Cases of natural amanitin toxicosis are reported in humans and dogs, and experimental toxicity studies have been described in a variety of species. 1,2,5,7,10 The clinical progression is classically described as multiphasic. 2,5,7,8,9 Following an initial latency period 6 to 24 hours post ingestion, gastrointestinal (GI) signs occur, including vomiting, bloody diarrhea, and abdominal pain. This can be followed by a period of seeming recovery, which may last hours to days, until the development of clinical signs of hepatic and renal failure in the final phase. Acute hepatocellular necrosis, often accompanied by renal proximal tubular epithelial necrosis, is the typical pathological finding. 2,5,7,8,9 We report the clinical and pathological changes associated with amanitin toxicosis in 2 cats. To our knowledge, this is the first report of amanitin toxicosis in cats. Cat No. 1In November, a 1-year-old spayed female domestic shorthair cat was presented to a veterinary practice in northern California for acute onset of vomiting, lethargy, and anorexia. Rectal temperature was 105.7 F. A complete blood count (CBC) was unremarkable. Serum chemistry abnormalities included marked elevation (too high to register) of alanine aminotransferase (ALT) and mild elevation of alkaline phosphatase (ALP) (128 IU/L; range 14-111 IU/L). Abdominal radiographs showed gas accumulation in the small intestine. An abdominal ultrasound showed a flaccid, fluid-filled stomach, hypermotile duodenum, and mild thickening of the colon wall. Treatment with ampicillin and supportive care was initiated. Fever and vomiting resolved, but anorexia continued and the patient became progressively depressed and developed ataxia and visual and proprioceptive deficits. After 48 hours, a repeat CBC was performed; the cat had thrombocytopenia (84 Â 1...

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“…The cycle peptide chain, α-amanitin, has eight amino acids: asparagine, hydroxyl proline, dihydroxy isoleucine, hydroxyl-mercapto-tryptophan, glycine, isoleucine, glycine and alanine. Hydroxyl proline and dihydroxy isoleucine activate RNA polymerase II and III by binding to the enzyme molecule, enhancing the activating effect by means of glycine and isoleucine binding [6][7][8]. The immediate cause of death from mushroom poisoning is kidney, liver and respiratory failure which occur within one week of ingestion.…”

Section: Introductionmentioning

confidence: 99%

Deactivation Study of α-Amanitin Toxicity in Poisonous Amanita spp. Mushrooms by the Common Substances In Vitro

Narongchai¹,

Narongchai²

2017

J Forensic Res

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The purpose of this research was to find out the substance which deactivate α-Amanitin ToxicityThe materials and methods used in the study include analysis with high performance liquid chromatography (HPLC) to:1.Demonstrate the standard α-amanitin at concentrations of 25, 50 and 100 µg/ml 2.Determine the deactivation of α-amanitin with 1) 18% acetic acid 2), calcium hydroxide 40 mg/ml, 3) potassium permanganate 20 mg/ml, 4) sodium bicarbonate 20 mg/ml 3.Report the statistical analysis as the mean ± standard deviation (SD) and paired t-test.The result revealed that potassium permanganate could eliminate 100 percent of the α-amanitin at 25, 50 and 100 µg/ml. Calcium hydroxide, sodium bicarbonate and acetic acid had lower elimination rates at those concentrations: 68.43 ± 2.58 (-71.4, -67.2, -66.7%), 21.48 ± 10.23 (-29.4, -25.2, -9.9%) and 3.21 ± 0.02% (-3.2, -3.2, +1.1%), respectively. The conclusion of this study was suggested that potassium permanganate could be applied as an absorbent substance during gastric lavage in patients with mushroom poisoning. It also might be effective as a cleansing wash for uncooked mushrooms. Investigation of potassium permanganate's ability to absorb α-amanitin in animal models and humans should be considered. .Patients with α-amanitin poisoning can develop severe toxic hepatitis, centrilobular necrosis, liver steatosis, and acute tubulointerstitial necrosis leading to hepatorenal syndrome all of which have a high mortality rate. The most effective treatment is emptying the stomach promptly by performing gastric lavage with 1:2,000 tannic acid or 1:10,000 potassium permanganase plus triggering emesis. A warm saline solution of potassium permaganase can be used as an emergency treatment to reduce toxins in the intestines and stomach. Thus, KMnO 4 , NaHCO 3 , Ca(OH) 2 and acetic acid should be considered as a cleanser for uncooked mushrooms to deactivate α-amanitin toxicity and potentially reduce the mortality rate from liver failure, acute renal failure, respiratory failure and gastro-intestinal haemorrhage [9]. Materials and MethodsIn this study, experiments were performed on α-amanitin at concentrations of 25, 50 and 100 µg/ml eached mixed with 1) 18% acetic acid 2), calcium hydroxide 40 mg/ml, 3) potassium permanganate 20 mg/ml, 4) sodium bicarbonate 20 mg/ml (results analyzed with high performance liquid chromatography (HPLC) with Luna C18 (150 × 4.6 mm I.D., 5 micron) from Phenomenex ® , USA), or 5) mobile phase (a mixture of 0.02 M aqueous ammonium acetate and acetonitrile (88/12, v/v) pH 5.0 at an absorbance of 280 nm). Glacial acetic acid was used to Citation: Narongchai P, Narongchai S (2017) Deactivation Study of α-Amanitin Toxicity in Poisonous Amanita spp. Mushrooms by the Common Substances In Vitro. J Forensic Res 8: 396.

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The toxic peptides from Amanita mushrooms

Cited by 143 publications

References 106 publications

Transcriptomic and proteomic analysis of global ischemia and cardioprotection in the rabbit heart

Transcriptomic and proteomic analysis of global ischemia and cardioprotection in the rabbit heart

Amanitin Toxicosis in Two Cats with Acute Hepatic and Renal Failure

Deactivation Study of α-Amanitin Toxicity in Poisonous Amanita spp. Mushrooms by the Common Substances In Vitro

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