Effects of vitamin E on microsomal Ca 2+ ‐ATPase activity and calcium levels in streptozotocin‐induced diabetic rat kidney

Vitamin E treatment has been found to be beneficial in preventing or reducing diabetic nephropathy. Increased tissue calcium and abnormal microsomal Ca 2+ ‐ATPase activity have been suggested as contributing factors in the development of diabetic nephropathy. This study was undertaken to test the hypothesis that vitamin E reduces lipid peroxidation and can prevent the abnormalities in microsomal Ca 2+ ‐ATPase activity and calcium levels in kidney of streptozotocin (STZ)‐induced diabetic rats. Male rats were rendered diabetic by a single STZ injection (55 mg kg −1 i.p.). After diabetes was verified, diabetic and age‐matched control rats were untreated or treated with vitamin E (400–500 IU kg −1  day −1 , orally) for 10 weeks. Ca 2+ ‐ATPase activity and lipid peroxidation (MDA) were determined spectrophotometrically. Blood glucose levels increased approximately five‐fold (> 500 mg dl −1 ) in untreated‐diabetic rats but decreased to 340±27 mg dl −1 in the vitamin E treated‐diabetic group. Kidney MDA levels did not significantly change in the diabetic state. However, vitamin E treatment markedly inhibited MDA levels in both control and diabetic animals. Ca 2+ ‐ATPase activity was 0.483±0.008 U l −1 in the control group and significantly increased to 0.754±0.010 U l −1 in the STZ‐diabetic group ( p  < 0.001). Vitamin E treatment completely prevented the diabetes‐induced increase in Ca 2+ ‐ATPase activity (0.307±0.025 U l −1 , p  < 0.001) and also reduced the enzyme activity in normal control rats. STZ‐diabetes resulted in approximately two‐fold increase in total calcium content of kidney. Vitamin E treatment led to a significant reduction in kidney calcium levels of both control and diabetic animals ( p  < 0.001). Thus, vitamin E treatment can lower blood glucose and lipid peroxidation, which in turn prevents the abnormalities in kidney calcium metabolism of diabetic rats. This study describes a potential biochemical mechanism by which vitamin E supplementation may delay or inhibit the development of cellular damage and nephropathy in diabetes. Copyright © 2003 John Wiley & Sons, Ltd.