Kidney Injury Induced by Lipid Peroxide Produced by Vitamin E Deficiency and GSH Depletion in Rats

Four-week-old Wistar male rats were fed a vitamin E (VE)-deficient (OE) or a VE-sufficient (10E) diet for 6 weeks and then intraperitoneally treated with buthionine sulfoximine (BSO) at 1mmol/kg body weight once a day for 3 days. Glutathione (GSH) depletion by BSO treatment caused injuries especiall...

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Bibliographic Details
Published in:Journal of Nutritional Science and Vitaminology 1991, Vol.37(1), pp.99-107
Main Authors: HAGIWARA, Kiyokazu, NAITO, Katsushi, KUROKAWA, Yuji, ICHIKAWA, Tomio
Format: Article
Language:English
Subjects:
Animals
Buthionine Sulfoximine
Diet
DL-buthionine sulfoximine
Glutathione - analysis
Glutathione - deficiency
GSH depletion
Histocytochemistry
Kidney - drug effects
Kidney - pathology
kidney injury
lipid peroxide
Lipid Peroxides - biosynthesis
Lipid Peroxides - pharmacology
Male
Methionine Sulfoximine - analogs & derivatives
Methionine Sulfoximine - toxicity
Rats
Rats, Inbred Strains
Vitamin E - analysis
vitamin E deficiency
Vitamin E Deficiency - metabolism
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Summary:Four-week-old Wistar male rats were fed a vitamin E (VE)-deficient (OE) or a VE-sufficient (10E) diet for 6 weeks and then intraperitoneally treated with buthionine sulfoximine (BSO) at 1mmol/kg body weight once a day for 3 days. Glutathione (GSH) depletion by BSO treatment caused injuries especially in the kidneys of VE-deficient rats. The kidney weight increased in the VE-deficient rats after BSO treatment (OE-BSO). It was observed that the epithelial cells of the renal tubules in this group were strongly impaired and the injuries were necrosis and desquamation. No injury was observed in the kidneys of the BSO-untreated 0E group and the 10E groups. The TBA value of the kidney of 0E-BSO group was lower than that of the BSO-untreated OE group, but the lipofuscin content of the kidney of the OE-BSO group was 10 times higher than that of the BSO-untreated 0E group. These results suggest that the kidney injuries in rats may be caused by lipid peroxidation induced by vitamin E deficiency and glutathione depletion.
ISSN:0301-4800
1881-7742
DOI:10.3177/jnsv.37.99