phalloidine and Mushroom-Poisoning

Acute liver failure is a rare disease that can cause death in the majority of untreated cases. Sudden loss of liver function in the absence of a preexisting liver disease is considered the true form and has to be distinguished from impaired function following exacerbation of an underlying liver disease (acute or chronic failure). Common causes include acute viral hepatitis, drug induced liver injury (DILI) and toxins. The loss of the excretory and synthetic function of the liver marks the clinical presentation and results in icterus, coagulopathy and encephalopathy. Additionally impairment of renal function and sepsis occur and contribute to the high mortality of this disease. The activation of cell death mechanisms (apoptosis) leading to a reductio of viable, functional liver tissue is considered to be an important pathophysiologic mechanism. Curative therapy of this disease includes liver transplantation that has been performed in Germany for the first time in 1969. In the year 2004 a total of 91 liver transplantation were performed for acute liver failure (10.3% of all transplants) in German transplant centers.

Topics: Acute Disease; Adolescent; Adult; Amanita; Anti-Bacterial Agents; Antidotes; Child, Preschool; Drug-Related Side Effects and Adverse Reactions; Germany; Hepatic Encephalopathy; Hepatitis A; Hepatitis B; Hepatitis C; Hepatitis D; Hepatitis E; Hepatocytes; Humans; Liver Failure, Acute; Liver Transplantation; Mushroom Poisoning; Phalloidine; Plasmapheresis; Prognosis; Renal Dialysis; Renal Insufficiency; Substance-Related Disorders

This paper examines the biology and medical consequences of ingesting the potentially lethal poisonous mushroom, Amanita virosa, the Destroying Angel. The fungus, its structure, distribution and toxic components are described. Symptoms of human poisoning by A. virosa are described, following the order of Homeopathic Repertories. Laboratory values for comparison with normal values of haematology, biochemistry and urine analyses are given.

Topics: Amanita; Amanitins; Humans; Materia Medica; Mushroom Poisoning; Phalloidine; Risk Factors

This paper examines the biology and medical consequences of ingesting the potential lethal poisonous mushroom, Amanita phalloides, the Death Cap. The organism is a fungus, its structure, distribution and toxic components are described. Symptoms of human poisoning by Am. phalloides are described, following the order of Homeopathic Repertories.

Topics: Amanita; Diagnosis, Differential; Humans; Materia Medica; Mushroom Poisoning; Phalloidine

The experimental basis for the treatment of death-cap poisoning is reviewed. The available data suggest penicillin and silymarin as the antidotes most likely to be effective. Measures to increase the elimination of the toxins appear to be warranted.

Topics: Amanita; Animals; Carbon Tetrachloride; Charcoal; Common Bile Duct; Cytochrome c Group; Drainage; Drug Synergism; Flavonoids; Humans; Mice; Mushroom Poisoning; Penicillins; Phalloidine; Phenylbutazone; Prednisolone; Rats; Renal Dialysis; Rifampin; Silymarin; Thioctic Acid

Pseudosperma species are widely distributed worldwide. Many of them cause poisoning incidents every year, and the toxin responsible for poisoning is muscarine, which could stimulate the parasympathetic nervous system. This study established a method using multiwalled carbon nanotube purification and liquid chromatography-tandem mass spectrometry for the targeted screening of mushroom toxins (muscarine, isoxazole derivatives, tryptamine alkaloids, three amatoxins and three phallotoxins) from Pseudosperma umbrinellum, a common poisonous mushroom distributed in north and northwestern China. Surprisingly, in addition to muscarine, phalloidin was also detected in P. umbrinellum, and the contents were 3022.2 ± 604.4 to 4002.3 ± 804.6 mg/kg (k = 2; p = 95%) muscarine and 5.9 ± 1.2 to 9.3 ± 1.8 mg/kg (k = 2; p = 95%) phalloidin.

Topics: Agaricales; Amanitins; Muscarine; Mushroom Poisoning; Phalloidine

Most of the fatal cases of mushroom poisoning are caused by Amanita phalloides. The amount of toxin in mushroom varies according to climate and environmental conditions. The aim of this study is to measure α-, β-, and γ-amanitin with phalloidin and phallacidin toxin concentrations. Six pieces of A. phalloides mushrooms were gathered from a wooded area of Düzce, Turkey, on November 23, 2011. The mushrooms were broken into pieces as spores, mycelium, pileus, gills, stipe, and volva. α-, β-, and γ-Amanitin with phalloidin and phallacidin were analyzed using reversed-phase high-performance liquid chromatography. As a mobile phase, 50 mM ammonium acetate + acetonitrile (90 + 10, v/v) was used with a flow rate of 1 mL/min. C18 reverse phase column (150 × 4.6 mm; 5 µm particle) was used. The least amount of γ-amanitin toxins was found at the mycelium. The other toxins found to be in the least amount turned out to be the ones at the spores. The maximum amounts of amatoxins and phallotoxin were found at gills and pileus, respectively. In this study, the amount of toxin in the spores of A. phalloides was published for the first time, and this study is pioneering to deal with the amount of toxin in mushrooms grown in Turkey.

Topics: Alpha-Amanitin; Amanita; Amanitins; Chromatography, High Pressure Liquid; Chromatography, Reverse-Phase; Forests; Fruiting Bodies, Fungal; Humans; Mushroom Poisoning; Mycelium; Peptides, Cyclic; Phalloidine; Species Specificity; Spectrophotometry, Ultraviolet; Spores, Fungal; Turkey

Accidental or deliberate poisoning of food is of great national and international concern. Detecting and identifying potentially toxic agents in food is challenging due to their large chemical diversity and the complexity range of food matrices. A methodology is presented whereby toxic agents are identified and further characterized using a two-step approach. First, generic screening is performed by LC/MS/MS to detect toxins based on a list of selected potential chemical threat agents (CTAs). After identifying the CTAs, a second LC/MS analysis is performed applying accurate mass determination and the generation of an attribution profile. To demonstrate the potential of the methodology, toxins from the mushrooms Amanita phalloides and Amanita virosa were analyzed. These mushrooms are known to produce cyclic peptide toxins, which can be grouped into amatoxins, phallotoxins and virotoxins, where α-amanitin and β-amanitin are regarded as the most potent. To represent a typical complex food sample, mushroom stews containing either A. phalloides or A. virosa were prepared. By combining the screening method with accurate mass analysis, the attribution profile for the identified toxins and related components in each stew was established and used to identify the mushroom species in question. In addition, the analytical data was consistent with the fact that the A. virosa specimens used in this study were of European origin. This adds an important piece of information that enables geographic attribution and strengthens the attribution profile.

Topics: Amanita; Amanitins; Chromatography, Liquid; Humans; Mass Spectrometry; Mushroom Poisoning; Peptides, Cyclic; Phalloidine; Poisons

Hepatocyte uptake of phalloidin is carried out mainly by OATP1B1. We have used this compound as a prototypic substrate and assayed the ability to inhibit OATP-mediated phalloidin transport of four bile acid derivatives (BALU-1, BALU-2, BALU-3 and BALU-4) that showed positive results in preliminary screening. Using Xenopus laevis oocytes for heterologous expression of transporters, BALUs were found to inhibit taurocholic acid (TCA) transport by OATP1B1 (but not OATP1B3) as well as by rat Oatp1a1, Oatp1a4 and Oatp1b2. The study of their ability to inhibit sodium-dependent bile acid transporters revealed that the four BALUs induced an inhibition of rat Asbt-mediated TCA transport, which was similar to TCA-induced self-inhibition. Regarding human NTCP and rat Ntcp, BALU-1 differs from the other three BALUS in its lack of effect on TCA transport by these proteins. Using HPLC-MS/MS and CHO cells stably expressing OATP1B1 the ability of BALU-1 to inhibit the uptake of phalloidin itself by this transporter was confirmed. Kinetic analysis using X. laevis oocytes revealed that BALU-1-induced inhibition of OATP1B1 was mainly due to a competitive mechanism (Ki=8 microM). In conclusion, BALU-1 may be useful as a pharmacological tool to inhibit the uptake of compounds mainly taken up by OATP1B1 presumably without impairing bile acid uptake by the major carrier accounting for this process, i.e., NTCP.

Topics: Animals; Bile Acids and Salts; Binding, Competitive; Biological Transport; CHO Cells; Cricetinae; Cricetulus; Female; Humans; In Vitro Techniques; Liver-Specific Organic Anion Transporter 1; Mushroom Poisoning; Oocytes; Organic Anion Transporters; Phalloidine; Rats; Taurocholic Acid; Transfection; Xenopus laevis

The identification of toxic oligopeptides employing CE-ESI-MS is presented. The analytes studied ama- and phallotoxins are of significant forensic interest because over 90% of the lethal cases of fungus poisoning in man are caused by species of Amanita which contain these toxins. A CE method was developed to separate the toxins alpha-, beta- and gamma-amanitin, phalloidin and phallacidin. Their fragmentation patterns in MS(n) experiments were investigated in the positive and in the negative ion mode, also the influence of the sheath liquid mixture of the used interface on the S/N. Method validation included the determination of the LOD and the repeatability of the migration time and peak area for both detection modes. With the optimized method LODs of 13-79 ng/mL (17-87 nmol/L) were reached. The CE-MS procedure was successfully applied to the identification of ama- and phallotoxins in extracts of air-dried mushroom samples.

Topics: Amanita; Amanitins; Electrophoresis, Capillary; Humans; Molecular Structure; Mushroom Poisoning; Mycotoxins; Oligopeptides; Peptides, Cyclic; Phalloidine; Spectrometry, Mass, Electrospray Ionization

After consumption of mushrooms containing amatoxins (Amanita, Lepiota, and Galerina species), symptoms usually develop after a long delay (>6 h). Initial symptoms start as severe gastroenteritis, progressing to liver failure and possibly death as a result of hepatic coma. Since the survival rate of poisoned patients is claimed to depend on the time of beginning of efficient treatment, fast and reliable assays for amatoxins in biological fluids are essential. Described analytical methods for amatoxins include high performance liquid chromatography and radioimmunoassay (RIA). Recently, a new enzyme-linked immunosorbent assay (Bühlmann Amanitin ELISA kit) has been introduced as an alternative method to RIA. This ELISA-based assay offers several advantages: no complex extraction procedure is required (vs. HPLC) and no safety precautions concerning radioactivity have to be taken (vs. RIA). From August 2004 to October 2005, a pilot study was performed to test the practicability and the clinical utility of this method in emergency situations.. ten urines, 9 serums and 1 faeces from 10 patients suffering from acute gastroenteritis after mushroom ingestions (7 contaminated meals) were analyzed. Definitive diagnosis of amatoxin poisoning was made in 4 cases (3 contaminated meals) on the basis of the anamnesis, laboratory results, and clinical course. A patient developed a severe amatoxin poisoning with urinary amanitins level < 1.5 microg/L (urines were collected more than 72 h after mushroom ingestion). Two patients were paucisymptomatic with urinary amanitins levels >10 microg/L (urines were collected before the 36th hour).. Urine is the sample of choice for the determination of amatoxins. The most critical factor to invalidate the usefulness of this analysis is time. After 36 h, the sensitivity is unreliable.

Topics: Amanitins; Enzyme-Linked Immunosorbent Assay; Female; Humans; Male; Mushroom Poisoning; Phalloidine; Syndrome

In the past 10 years from 1991 to 2000, the number of consultations to the Japan Poison Information Center were 947 concerning mushroom poisonings. However, those from the hospital cases were not analyzed toxicologically. We examined toxicologically 20 cases (35 patients) of mushroom poisonings from 1993 to 2001. Investigation of amanita toxin poisoning was requested in 19 cases. We could detect the amanita toxin, amanitin, and phalloidin, in two cases, which resulted in concluding the cause of death. A fatal case by the magic mushroom poisoning was analyzed in the blood, urine, and mushroom, and we detected the hallucinogenic substances from the body fluids and ingested mushrooms. We report the results of our examinations, and point out the usefulness of the examination of the mushroom itself and biological samples toxicologically for forensic practice.

Topics: Adult; Aged; Amanita; Amanitins; Chromatography, High Pressure Liquid; Gas Chromatography-Mass Spectrometry; Humans; Japan; Male; Mushroom Poisoning; Phalloidine

Forty-eight hours after a women was poisoned by ingesting Amanita phalloides mushrooms, she developed fulminant hepatic failure with collapse, pH 7.24, lactic acidosis 7.6 mmol/l, hypoglycaemia 3.5 mmol/l, anuria and stage IV coma requiring tracheal intubation and mechanical ventilation. Transaminase level was up to 8,000 UI/l. Prothrombin and factor V levels were below 10 percent, with an APT time of 86 s versus a 29 s control time. Twenty-four hours after her admission, the patient underwent orthotopic liver transplantation. The postoperative period was uneventful, with return to consciousness and rapid normalization of hepatic biochemistry values, without signs of acute rejection. This 10th published case of orthotopic liver transplantation for Amanita phalloides poisoning with acute hepatic necrosis confirms that this type of treatment must be systematically envisaged in all such cases.

Topics: Amanita; Amanitins; Chemical and Drug Induced Liver Injury; Female; Humans; Liver Transplantation; Middle Aged; Mushroom Poisoning; Phalloidine

Topics: Acute Disease; Amanita; Amanitins; Child, Preschool; Gallbladder; Humans; Male; Mushroom Poisoning; Phalloidine; Ultrasonography

A reversed-phase high-performance liquid chromatographic assay has been developed for the simultaneous determination of alpha-amanitin and phalloidin in human plasma. The procedure is based on the enrichment of the toxins on a pre-column, followed by the transfer of both compounds in a foreflush mode to the analytical column. alpha-Amanitin and phalloidin can be quantified reliably down to a minimum concentration of 10 ng/ml in plasma (relative standard deviation less than 10%). An alternative method is recommended for hepatic coma patients.

Topics: Agaricales; Amanita; Amanitins; Child; Humans; Indicators and Reagents; Mushroom Poisoning; Oligopeptides; Phalloidine; Solvents

The phalloidine mushroom poisoning is an exogenic intoxication with specific action of the mushroom toxins on the liver and its functions. The dynamic follow up of serum cholinesterase activity in patients with phalloidine intoxication revealed that it was significantly decreased in the patients who died in comparison to those who survived. In the patients who survived and recovered the serum cholinesterase was moderately decreased and later increased. As a protein product synthesized in the liver the serum cholinesterase is a good marker of the protein-synthesizing function of the liver in patients with phalloidine intoxication and may be used as a prognostic test for its outcome.

Topics: Acute Disease; Adolescent; Adult; Cholinesterases; Clinical Enzyme Tests; Humans; Middle Aged; Mushroom Poisoning; Oligopeptides; Phalloidine; Prognosis; Time Factors

The liver functional disorders and structural changes were studied in 17 patients (children 6, adults 11, 4 to 70 years of age) with phalloidine intoxication. The clinical course of this severe and lethal exogenic intoxication, its characteristic clinical and laboratory features are discussed in relation to the morphological changes of the liver. The structural changes are similar in all patients independently of their age and the time of death. They are presented by fatty degeneration, acute toxic liver dystrophy and centrilobular necroses. These changes are produced by the specific action of the phalloidine toxins on the liver.

Topics: Adolescent; Adult; Aged; Amanita; Child; Child, Preschool; Humans; Liver; Microscopy, Electron; Middle Aged; Mushroom Poisoning; Phalloidine

In contrast to popular opinion phallotoxins do not play a role in poisoning with Amanita phalloides when the fungi are ingested orally. All toxic properties of this mushroom are due to amatoxins which, in contrast to the phallotoxins, are absorbed upon ingestion. Nearly all experiments on intact animals were performed by parenteral injection of phalloidin and therefore, most of these are unsuitable for practical consideration. In the present survey, however, a series of important findings are discussed, which provide insight into various functions of liver cells. When present in the blood, phalloidin and other phallotoxins are selectively taken up by hepatocytes. No other types of cells are sensitive to the toxin. No extrahepatic tissue is primarily impaired by phalloidin. Phalloidin cannot be degraded by peptidases or by proteases occurring in animals. Phalloidin is therefore a useful model substance for studies on the uptake of cyclopeptides by liver cells. The carrier system responsible for the active uptake of phalloidin can also translocate antamanide and several cyclic modifications of somatostatin. Phallotoxins bind with high affinity to microfilamentous structures, in particular to F-actin [Govindan et al., Naturwissenschaften, 59 (1972) 521-522] whereas phallotoxins are not bound to the monomer (G-actin). With respect to the strong organotropism of phallotoxins, intravenously injected phalloidin binds preferentially to microfilamentous F-actin of hepatocytes. Phalloidin is therefore a tool for inactivation of microfilamentous functions specifically in liver cells, and is suitable as a prototype of a cholestatic agent. In perfused livers arrest of bile flow is the earliest effect seen after addition of the toxin. In cells from other tissues phalloidin is only toxic when applied by intracellular microinjection. Phalloidin poisoning has been often used as a model for liver damage in the testing of hepatoprotective drugs. This substance is, however, not useful for such studies since the mechanism of phalloidin poisoning is too specific for interpretation in the sense of general liver protection.

Topics: Actin Cytoskeleton; Amanita; Amanitins; Animals; Bile; Chemical Phenomena; Chemistry; Liver; Mice; Mushroom Poisoning; Oligopeptides; Phalloidine; Rats

Survival of mice after lethal doses of a lyophilizate from Amanita phalloides ('death cap') was markedly increased by single doses of ethanol applied 30 min before or 5 min after the mushroom. Hepatic histopathological damage (confluent necrosis) was largely prevented. Acute, but not chronic, consumption of ethanol may thus influence favorably the outcome of death cap poisoning and should be taken into consideration in the evaluation of therapeutic measures.

Topics: Amanita; Amanitins; Animals; Drug Interactions; Ethanol; Female; Liver; Mice; Mushroom Poisoning; Mycotoxins; Phalloidine

Topics: Amanita; Amanitins; Humans; Liver; Mushroom Poisoning; Mycotoxins; Phalloidine

An analysis of 28 cases of amanita phalloides poisoning serves as basis for a discussion of the clinical features and therapeutic problems involved. A critical review of recent experimental investigations in animals points to new possibilities in the treatment of amanita phalloides poisoning.

Topics: Adult; Amanita; Amanitins; Austria; Chemical and Drug Induced Liver Injury; Child; Exchange Transfusion, Whole Blood; Female; Humans; Male; Mushroom Poisoning; Phalloidine; Prothrombin; Renal Dialysis; Vitamin K

2,4-Monofurfurylidene-tetra-O-methyl sorbitol (MSF), which prevents hepatotoxic effects of amanita phalloides powder (APP) in mice and of CCl4 in rats, increases liver microsomal drug-metabolizing activity in mice, as shown by a) the prolongation of pentobarbital or zoxazolamine-induced loss of the righting reflex and b) the decrease of phenylbutazone plasma levels. Further phenobarbital sodium, administered according the schedule usual for liver microsomal drug-metabolizing enzyme induction, also protects mice from APP death. On the other hand 2-diethylamino-ethyl-2,2-diphenylvalerate HCl (SKF 525-A) aggravates APP-toxicity and reduces APP protection afforded by both MSF and phenobarbital. Since it has been widely recognized that liver microsomal drug-metabolizing enzymes toxify phalloidin as well as CCl4, it is suggested that 1. mice APP toxicity depends on an unknown factor similar to but not identical to phalloidin, 2. MSF-antitoxic effect is produced by a mechanism unrelated to stimulation of liver microsomal drug-metabolizing system.

Topics: Amanita; Animals; Endoplasmic Reticulum; Female; Furans; Liver; Mice; Mushroom Poisoning; Phalloidine; Phenobarbital; Proadifen; Rats; Sorbitol; Time Factors

The effect Amanita phalloides on glucose tolerance and insuline sensitivity was studied. Amanita phalloides toxins were injected to albino male rats intraperitoneally in a dose of DL50. Amanita phalloides proved to cause disturbance of glucose tolerance, increased tissue glucose utilization, and enhanced the organism insuline sensitivity. The mentioned effects result from a decrease of insuline-inactivating capacity of the liver and from enhanced function of the insuline apparatus of the pancreas.

Topics: Amanita; Animals; Blood Glucose; Glucose Tolerance Test; Insulin; Male; Mushroom Poisoning; Phalloidine; Rats

Topics: Animals; Arginine; Chemical and Drug Induced Liver Injury; Liver; Male; Mushroom Poisoning; Oligopeptides; Perfusion; Phalloidine; Potassium Deficiency; Rats

Topics: 4-Aminobenzoic Acid; Amanitins; Amino Acids, Sulfur; Aminobenzoates; Aminocaproates; Aminocaproic Acid; Animals; Antidotes; Benzopyrans; Catechin; Flavonoids; Mice; Mushroom Poisoning; Oligopeptides; Phalloidine; Pyridines; Silymarin; Tiopronin

The effectiveness of three plasma cleansing techniques (exchange transfusion, peritoneal dialysis and plasmapheresis) is studied in the treatment of phalloides intoxication. The severity of the latter is dependent upon the amount of toxin ingested, with can now be measured by radio-immunology, as well as the fixation of the toxin in the liver. Methods to ensure its elimination must be instituted as soon as possible. Thus in 43 patients who had consumed more than 50 g of fresh fungi, there were no deaths amongst those treated during the first 36 hours and 7 deaths out of 22 patients treated late. It is not yet possible to define the respective values of each method.

Topics: Adolescent; Adult; Agaricales; Aged; Amanita; Amanitins; Blood Transfusion; Body Weight; Child; Child, Preschool; Female; Humans; Male; Middle Aged; Mushroom Poisoning; Oligopeptides; Peritoneal Dialysis; Phalloidine; Radioimmunoassay; Time Factors

Topics: Amanita; Animals; Flavonoids; Lethal Dose 50; Mice; Mushroom Poisoning; Oligopeptides; Phalloidine; Rats; Silymarin; Time Factors

Topics: Alanine Transaminase; Amanita; Animals; Aspartate Aminotransferases; Ethanol; Ethionine; Female; Flavonoids; L-Lactate Dehydrogenase; Liver; Malate Dehydrogenase; Male; Mice; Mushroom Poisoning; Oligopeptides; Phalloidine; Polyvinylpyridine N-Oxide; Polyvinyls; Rats; Salts; Silymarin; Succinate Dehydrogenase; Triglycerides

The protective action of dibenzothioline and silymarin in the acute intoxication by phalloidin and alpha-amanitin has been studied on the basis of their ability to attenuate changes in dry mass distribution and class-pattern of the hepatocytes, as evaluated by microinterferometry. Protective agents were given to male rats 30 min before toxin, and the animals were sacrificed 3.0 h later. Both dibenzothioline and silymarin markedly counteract the toxic action of phalloidin and alpha-amanitin on the hepatocyte population, as revealed by a substantial prevention (a) of the striking displacement of hepatocytes in the intervals among the classes as regards phalloidin poisoning, and (b) of the number decrease of hepatocyte classes due to disappearance of the heaviest ones, of the shift of hepatocytes to the lighter classes, of the appearance of very light cells, of the displacement of hepatocytes into the class intervals and of the decrease in nuclear dry mass as regards alpha-amanitin. It is suggested that dibenzothioline and silymarin exert their protective action by a non-specific stabilization of the cell membrane.

Topics: Amanitins; Amino Acids, Sulfur; Animals; Cell Membrane; Flavonoids; Liver; Male; Mushroom Poisoning; Oligopeptides; Phalloidine; Pyridines; Rats; Silymarin

Agents with antagonistic effects against phalloidin or alpha-amanitin were tested in mice against lethal doses of an extract from the whole mushroom Amanita phalloides. The following categories of agents reduced lethality after the extract. First, agents protecting only against phalloidin such as rifampicin, phenylbutazone and antamanide. Second, silymarin and prednisolone which display both antiamatoxic and marked (silymarin) or moderate (prednisolone) anti-phallotoxic acitivty. Thioctic acid displayed some activity when tested against mid-lethal doses of the extract. Cytochrome c, a chemical with curative potencies against alpha-amanitin did not reduce the lethality of the exact. All of the effective agents acted only when applied prior to the poisoning. The pattern or protective activity would indicate that in mice death after single doses of Amanita phalloides may follow a qualitatively particular couse which is difficult to ascribe to phallo- or amatoxic effects alone.

Topics: Agaricales; Amanita; Amanitins; Animals; Antidotes; Carbon Tetrachloride; Cytochrome c Group; Female; Mice; Mushroom Poisoning; Peptides, Cyclic; Phalloidine; Phenylbutazone; Plant Extracts; Prednisolone; Rifampin; Silymarin; Thioctic Acid

Topics: Adult; Agaricales; Aged; Amanita; Amanitins; Chemical and Drug Induced Liver Injury; Female; Humans; L-Lactate Dehydrogenase; Male; Middle Aged; Mushroom Poisoning; Oligopeptides; Phalloidine

30 min after poisoning with Amanita phalloides extract or phalloidin, rat liver polyribosomes appear strongly dissociated, and a small increase of free phosphatase activity is evident. A cycloheximide pretreatment prevents the polyribosome dissociation, without protecting against the lysosomal change. This indicates that the polysomal derangement is not due to a hydrolytic breakdown of messenger RNA. Phalloidin, added in vitro either to a liver cell-free system, or to isolated hepatocytes, does not inhibit their amino acid incorporating activity. The polysome dissociation, therefore, is dependent on changes induced by phalloidin when the liver cell is "in situ".

Topics: Agaricales; Amanita; Amino Acids; Animals; Cell-Free System; Liver; Lysosomes; Male; Mushroom Poisoning; Oligopeptides; Phalloidine; Polyribosomes; Protein Biosynthesis; Rats; Time Factors

Topics: Agaricales; Amanita; Amanitins; Humans; Male; Mushroom Poisoning; Oligopeptides; Phalloidine