human hepatocyte culture intoxicated with a-amanitin a-Amanitin (a-AMA) is the main toxin of Amanita phalloides and its subspecies (A. virosa and A. verna). The primary mechanism of a-AMA toxicity is associated with protein synthesis blocking in hepatocytes. Additionally, a-AMA exhibits prooxidant properties that may contribute to its severe hepatotoxicity. The aim of the present study was to assess the effect of a-AMA on lipid peroxidation and the activities of superoxide dismutase (SOD) and catalase (CAT) in human hepatocyte culture. The effects of benzylpenicillin (BPCN), N-acetyl-L-cysteine (ACC), and silibinin (SIL) on SOD and CAT activities and on lipid peroxidation in human hepatocyte culture intoxicated with a-AMA were also examined. In human hepatocyte culture, 48-hour expo- sure to a-AMA at a 2-mM concentration caused an increase in SOD activity, a reduction of CAT activity, and a significant increase in lipid peroxidation. Changes in SOD and CAT activity caused by a-AMA could probably enhance lipid peroxidation by increased generation of hydrogen peroxide combined with reduced detoxifica- tion of that oxygen radical. The addition of antidotes (ACC or SIL) to the culture medium provided more effective protection against lipid peroxidation in human hepatocytes intoxicated with a-AMA than the addition of BPCN, possessing no antioxidant properties.Death cap (Amanita phalloides) and its subspecies; death angel (Amanita virosa) and destroying angel (Amanita verna), are responsible for 95% of all mushroom-related deaths.1 The three species contain two main groups of toxins in their tissues, namely phallotoxins and amatoxins, which are both multicyc- lic peptides.
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