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- W1978018003 abstract "Thioacetamide induced a severe perivenous necrosis followed by a hepatocellular regenerative response, when administered in a single dose of 6.6 mmol/kg to rats. As (Ca2+)i plays an important role in both toxic cell killing and cell proliferation, the disturbances in the basal cytosolic calcium as well as the levels of Ca2+ sequestered in the endoplasmic reticulum were determined in hepatocytes isolated at 0, 12, 24, 48 and 72 h after thioacetamide administration. The basal Ca2+ increased progressively, reaching a maximum at 24 h of the intoxication (205%, p < 0.001), while the microsomal sequestered Ca2+ decreased at 24 h to 16% (p < 0.001) when compared with untreated controls. Changes in the activity of glycogen phosphorylase alpha paralleled those of basal free calcium and showed the maximum value also at 24 h (291%; p < 0.001). Moreover, there was a close association in time between the basal concentration of Ca2+ and the inhibition of microsomal Ca(2+)-dependent ATPase activity.The significant decrease in the levels of GSH and protein thiols indicates that oxidative stress is involved in thioacetamide-induced cell injury, but these decreases did not precede changes in cytosolic Ca2+ level. In the sequence of events leading to hepatic cell injury and regeneration, thioacetamide mobilized hepatic (Ca2+)i via inhibition of microsomal Ca(2+)-ATPase which may have activated Ca(2+)-dependent mechanisms involved both in cell death and in acute mitogen response." @default.
- W1978018003 created "2016-06-24" @default.
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- W1978018003 date "1996-04-01" @default.
- W1978018003 modified "2023-10-01" @default.
- W1978018003 title "Intracellular calcium concentration impairment in hepatocytes from thioacetamide-treated rats. Implications for the activity of Ca2+-dependent enzymes" @default.
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- W1978018003 doi "https://doi.org/10.1016/s0168-8278(96)80167-x" @default.
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