Previous studies have shown that reduction of renal mass in the rat remnant
kidney model induces overproduction of transforming growth factor beta 1 (
TGF beta 1). We investigated whether an antioxidant, vitamin E, administere
d before the renal mass reduction, could prevent oxidative stress, reduce t
he overproduction of TGF beta 1, and mitigate against the subsequent glomer
ulosclerosis. Our results revealed that the oxidative stress, as measured b
y the change in plasma malondialdehyde, is significantly reduced by prior v
itamin E dietary supplementation. Finally, our data show that dietary vitam
in E supplementation ameliorates the rise in TGF beta 1 secondary to renal
mass reduction and inhibits the glomerular sclerosis of the remnant kidney
over the time course of this experiment.