Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0022672 (acute tubular necrosis)
 2,175 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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 gamma-glutamylcysteine synthetase, at the dose of 1 mmol/kg body weight. As we reported previously, GSH depletion by administration of BSO induced acute tubular necrosis in the kidney of VE-deficient rats and was accompanied by decrease of renal TBA value and marked increase of renal lipofuscin content. In this study, we examined the effect of administration of AsA or Trolox C on these kidney injuries. AsA or Trolox C treatment increased renal GSH content and inhibited the increase of renal lipofuscin production. The increase of BUN and creatinine levels and LDH activity in the sera of rats administered BSO were inhibited by AsA or Trolox C treatment. AsA treatment completely protected the necrosis of epithelia of proximal renal tubules. These results suggest that GSH has an important role in preventing lipofuscin production through the reaction of lipid peroxides with amino acids. AsA spares GSH indicating that these compounds have similar antioxidant actions and that AsA can serve as an essential antioxidant in the presence of severe GSH deficiency.
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PMID:[Induction and prevention of kidney injury induced by GSH depletion and vitamin E deficiency in rats]. 781 39