We have evaluated the effect of dietary
antioxidant,
antioxidant biofactor (a processed grain food), on
iron nitrilotriacetate-induced renal
tumorigenesis, hyperproliferative response, and oxidative damage. In
tumorigenesis studies,
iron nitrilotriacetate alone treatment resulted in a development of 75% renal cell
tumor incidence, whereas, in the group of animals fed with
antioxidant biofactor diet and treated with
iron nitrilotriacetate, only 43% of renal cell
tumor incidence was observed. In oxidative damage studies, the decrease in the level of renal
glutathione and
antioxidant enzymes induced by
iron nitrilotriacetate was significantly reversed by
antioxidant biofactor diet pretreatment in a dose-dependent manner (18-71% recovery, P < 0.05).
Antioxidant biofactor diet pretreatment also resulted in a dose-dependent inhibition (35-49% inhibition, P < 0.05) of
iron nitrilotriacetate-induced lipid peroxidation as measured by
thiobarbituric acid reactive substances formation in renal tissues. Similarly, in hyperproliferation studies,
antioxidant biofactor diet pretreatment showed a strong inhibition of
iron nitrilotriacetate-induced renal
ornithine decarboxylase activity (18-54% inhibition, P < 0.05). In addition,
antioxidant biofactor fed diet pretreatment also protected the kidney tissues against observed histopathological alterations. From this data, it can be concluded that
antioxidant biofactor diet can abrogate the toxic and
tumor promoting effects of
iron nitrilotriacetate and can serve as a potent chemopreventive agent to suppress
oxidant-induced tissue injury and
tumorigenesis.