ビタミンＥ欠乏ラットのグルタチオン低下に伴う腎臓障害とグルタチオンエステル投与による防御

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  • Kidney Injury Induced by GSH Depletion and Vitamin E Deficiency in Rats and Prevention by GSH Ester Administration.
  • ビタミン E ケツボウ ラット ノ グルタチオン テイカ ニ トモナウ ジンゾ

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Four-week-old male Wistar 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 l mmol/kg body weight. Rats in a glutathione (GSH) treatment group were intraperitoneally injected three times with GSH monoisopropyl ester at 1.7 mmol/kg body weight in addition to BSO administration. The TBA (2-thiobarbituric acid) value, GSH content, lipofuscin content and enzyme activities in the kidneys of rats, and BUN (blood urea nitrogen) content, creatinine content and LDH (lactate dehydrogenase) activity in their sera were measured. GSH depletion by BSO administration was accompanied by a decrease in the renal TBA value and a marked increase in the renal lipofuscin content. This increase in the renal lipofuscin content was 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. GSH treatment did not completely prevent necrosis of the proximal renal tubule epithelia but such degeneration in rats treated with GSH was observed only in a narrow zone of the S3 segment near the descending thin limb of Henle's loop. It seems that lipid peroxides produced by VE deficiency may cause the accumulation of lipofuscin in the presence of renal GSH depletion, followed by necrosis of the proximal renal tubule epithelia. These results suggest that GSH has an important role in preventing the production of lipofuscin by reaction of lipid peroxides with amino acids.

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