Author(s): Vadivelan R, Umasankar P, Dipanjan Mandal, Shanish A, Dhanabal S.P, Elango K.

Email(s): rv_sofia@rediffmail.com

DOI: Not Available

Address: Vadivelan R, Umasankar P, Dipanjan Mandal, Shanish A, Dhanabal S.P and Elango K
Department of Pharmacology, J.S.S College of Pharmacy, (Off campus of JSS University, Mysore) Ooty, Niligiris-643001
*Corresponding Author

Published In:   Volume - 2,      Issue - 5,     Year - 2010


ABSTRACT:
Diabetic nephropathy is one of the main causes of renal end-stage disease. Morphologically, the development of diabetic nephropathy is characterized by progressive thickening of the glomerular basement membrane and by expansion of the mesangial matrix which correlates to glomerular filtration function. Hyperglycemia generates more reactive oxygen species and also attenuates antioxidative mechanisms through glycation of the scavenging enzymes. Therefore, oxidative stress has been considered to be a common pathogenetic factor of the diabetic complications including nephropathy. A causal relationship between oxidative stress and diabetic nephropathy has been established by observations that (1) Lipid peroxides and 8-hydroxydeoxyguanosine, indices of oxidative tissue injury, were increased in the kidneys of diabetic rats with albuminuria.(2) High glucose directly increases oxidative stress in glomerular mesangial cells, a target cell of diabetic nephropathy.(3) oxidative stress induces mRNA expression of TGF-b1(transforming growth factor beta1) and fibronectin which are the genes implicated in diabetic glomerular injury, and (4) Inhibition of oxidative stress ameliorates all the manifestations associated with diabetic nephropathy.


Cite this article:
Vadivelan R, Umasankar P, Dipanjan Mandal, Shanish A, Dhanabal SP, Elango K.Oxidative Stress Induced Diabetic Nephropathy. Research J. Pharmacology and Pharmacodynamics. 2010; 2(5): 321-323.


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