Portal de Periódicos da CAPES

Chloroacetamide hepatotoxicity: Hydropic degeneration and lipid peroxidation

1980; Elsevier BV; Volume: 55; Issue: 2 Linguagem: Inglês

10.1016/0041-008x(80)90089-7

1096-0333

Iréne Anundi, Jovan Rajs, Johan Högberg,

Liver Disease and Transplantation

Rats were treated with chloroacetamide (75 mg/kg) to rapidly deplete hepatic glutathione (GSH) and induce lipid peroxidation. Three to six hours after administration of chloroacetamide, midzonal and peripheral lesions developed in the liver parenchyma, and during this period an enhancement of lipid peroxidation [measured as thiobarbituric acid (TBA)-reacting material in liver homogenate] was seen. Reversible morphological changes, notably hydropic degeneration, were also seen at 24 and 48 hr. After 1 week no sign of regenerative growth in the liver was observed. TBA values remained high for up to 24 hr and then decreased to normal levels at 48 hr. The GSH content rapidly decreased; less than 10% remained after 1 hr and thereafter a progressive increase was seen with values slightly higher than normal observed at 48 and 72 hr. Rats fasted overnight were more susceptible to chloroacetamide toxicity and midzonal necrosis and higher TBA values were observed in those rats. The morphological changes were also more severe in rats treated with a higher dose (112.5 mg/kg) of chloroacetamide. The results indicate that hepatic GSH depletion leads to lipid peroxidation in vivo. They further suggest that lipid peroxidation can be significantly increased without causing permanent damage to the hepatocytes.