Kidney injury induced by lipid peroxide produced by vitamin E deficiency and GSH depletion in rats.

Abstract

Four-week-old Wistar male rats were fed a vitamin E (VE)-deficient (0E) or a VE-sufficient (10E) diet for 6 weeks and then intraperitoneally treated with buthionine sulfoximine (BSO) at 1 mmol/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 (0E-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 0E group, but the lipofuscin content of the kidney of the 0E-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.

• Authors: K Hagiwara, K Naito, Y Kurokawa, T Ichikawa
• Journal: Journal of nutritional science and vitaminology (J Nutr Sci Vitaminol (Tokyo)) Vol. 37 Issue 1 Pg. 99-107 (Feb 1991) ISSN: 0301-4800 [Print] Japan
• PMID: 1880635 (Publication Type: Journal Article)

Chemical References

• Lipid Peroxides
• Vitamin E
• Methionine Sulfoximine
• Buthionine Sulfoximine
• Glutathione

Topics

• Animals
• Buthionine Sulfoximine
• Diet
• Glutathione (analysis, deficiency)
• Histocytochemistry
• Kidney (drug effects, pathology)
• Lipid Peroxides (biosynthesis, pharmacology)
• Male
• Methionine Sulfoximine (analogs & derivatives, toxicity)
• Rats
• Rats, Inbred Strains
• Vitamin E (analysis)
• Vitamin E Deficiency (metabolism)