Evaluation of the fluidity and functionality of the renal cortical brush border membrane in experimental diabetes in rats.
The present study was aimed at addressing the effect of hyperglycemia on the renal cortical brush border membrane. The fluidity and the functionality of the renal cortical brush border membrane have been evaluated after 6 weeks of streptozotocin-induced diabetes in rats. Lipid peroxidation and protein oxidation were first performed to confirm a state of oxidative stress. The fluidity of the brush border membrane of diabetic rats decreased significantly by 15.76%. There was an increase in the amount of early (19.39%) and advanced (42.23%) glycation end-products suggesting the accumulation of significant amount of non-enzymic glycation products at 6 weeks of diabetes. Although, the activities of both gamma-glutamyl transpeptidase and alkaline phosphatase of the brush border membrane decreased, that of the latter decreased to a significant extent with an increase in K(m) (81%) and no change in the V(max). A study of the activities of glutathione-dependent antioxidant enzymes in the renal cortical homogenates showed that the activities of glutathione peroxidase and glyoxalase II were altered significantly. Our study seems to suggest that increased free radical generation accompanied by non-enzymic glycation may be responsible for oxidative stress and an increased rigidity of the diabetic brush border membrane. Alkaline phosphatase may thus serve as a potentially useful marker of free radical induced damage to the renal cortical brush border membrane. The results also suggest that enhanced susceptibility to oxidative stress during early stages may be an important factor in the development of secondary complications of diabetes.
Limaye
Pallavi V
PV
Department of Life Sciences, University of Mumbai, Santacruz (E), India.
Sivakami
S
S
D000818:Animals; D003921:Diabetes Mellitus, Experimental / Q000378:metabolism* / Q000473:pathology; D004950:Esterases / Q000378:metabolism; D017127:Glycation End Products, Advanced / Q000378:metabolism; D006943:Hyperglycemia / Q000378:metabolism; D007672:Kidney Cortex / Q000378:metabolism* / Q000648:ultrastructure*; D007791:Lactoylglutathione Lyase / Q000378:metabolism; D015227:Lipid Peroxidation / Q000502:physiology; D008297:Male; D008560:Membrane Fluidity / Q000502:physiology*; D008871:Microvilli / Q000378:metabolism; D018384:Oxidative Stress / Q000502:physiology; D010088:Oxidoreductases / Q000378:metabolism; D051381:Rats; D017208:Rats, Wistar; D005723:gamma-Glutamyltransferase / Q000378:metabolism
D017127:Glycation End Products, Advanced; D010088:Oxidoreductases; D005723:gamma-Glutamyltransferase; D004950:Esterases; D007791:Lactoylglutathione Lyase