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• W2011606516 abstract "Previously we showed that the redox active Cu(2+) was much more effective than Cd(2+) at inducing reactive oxygen species (ROS) formation in hepatocytes and furthermore ROS scavengers prevented Cu(2+)-induced hepatocyte cytotoxicity (Pourahmad and O'Brien, 2000). In the following it is shown that hepatocyte cytotoxicity induced by Cu(2+), but not Cd(2+), was preceded by lysosomal membrane damage as demonstrated by acridine orange release. Cytotoxicity, ROS formation, and lipid peroxidation were also readily prevented by methylamine or chloroquine (lysosomotropic agents) or 3-methyladenine (an inhibitor of autophagy). Hepatocyte lysosomal proteolysis was also activated by Cu(2+), but not Cd(2+), as tyrosine was released from the hepatocytes and was prevented by leupeptin and pepstatin (lysosomal protease inhibitors). Cu(2+)-induced cytotoxicity was also prevented by leupeptin and pepstatin. A marked increase in Cu(2+)-induced hepatocyte toxicity also occurred if the lysosomal toxins gentamicin or aurothioglucose were added at the same time as the Cu(2+). Furthermore, destabilizing lysosomal membranes beforehand by preincubating the hepatocytes with gentamicin or aurothioglucose prevented Cu(2+)-induced hepatocyte cytotoxicity. It is proposed that Cu(2+)-induced cytotoxicity involves lysosomal damage that causes the release of cytotoxic digestive enzymes as a result of lysosomal membrane damage by ROS generated by lysosomal Cu(2+) redox cycling." @default.
• W2011606516 created "2016-06-24" @default.
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• W2011606516 date "2001-01-01" @default.
• W2011606516 modified "2023-09-24" @default.
• W2011606516 title "Lysosomal involvement in hepatocyte cytotoxicity induced by Cu2+ but not Cd2+" @default.
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• W2011606516 doi "https://doi.org/10.1016/s0891-5849(00)00450-0" @default.
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