1992 Volume 45 Issue 1 Pages 55-60
Four-week-old Wistar male rats were fed a vitamin E (VE) -deficient diet for 8 weeks, followed by intraperitoneal injection of DL-buthionine- [S, R] -sulfoximine (BSO), an inhibitor of γ-glutamylcysteine synthetase, at 1mmol/kg body weight once a day for 3 days. Rats in a glutathione (GSH) treatment group were injected intraperitoneally with GSH monoisopropyl ester at 2.5mmol/kg body weight twice a day for 3 days in addition to BSU administration. The TBA (2-thiobarbituric acid) value, GSH conetnt, lipofuscin content and enzyme activities in the kidneys of rats, and BUN (blood urea nitrogen) content, creatinine conent and LDH (lactate dehydrogenase) activity in their sera were measured. GSH depletion by BSO administration decreased the renal TBA value, and increased markedly the renal lipofuscin content, The increase of renal lipofuscin was partly prevented by GSH treatment. The increase in serum creatinine and the decrease in renal enzyme activities of rats administered BSO were inhibited by GSH treatment, but the treatment could not completely protect against necrosis of the proximal renal tubule epithelia. It appears that lipid peroxides produced by VE deficiency may cause the accumulation of lipofuscin under renal GSH depletion, followed by necrosis of the proximal renal tubule epithelia. These results suggest that GSH has an important role in preventing lipofuscin production through the reaction of lipid peroxides with amino acids.
