Abrogation of DEN/Fe-NTA induced carcinogenic response, oxidative damage and subsequent cell proliferation response by Terminalia chebula in kidney of Wistar rats

In an effort to identify a new chemopreventive agent, the present study was conducted to investigate the role of T chebula in the prevention of ferric nitrilotriacetic acid (Fe- NTA) induced oxidative stress and renal tumorigenesis in Wistar rats. A single application of Fe-NTA (9 mg Fe/kg body weight, intraperitoneally) significantly induced oxidative stress and elevated the marker parameters of tumor promotion. However, the pretreatment of animals with different doses of T chebula extract (25 and 50 mg/kg body weight) restored the levels of reduced glutathione (GSH) and cellular protective enzymes (p < 0.05). Concomitantly, malondialdehyde (MDA) formation and hydrogen peroxide content were also reduced significantly (p < 0.05) at both the doses. The promotion parameters tested (ornithine decarboxylase activity and DNA synthesis) were also significantly suppressed (p < 0,05), T. chebula also inhibited N-diethyl nitrosamine initiated renal carcinogenesis by showing reduction in the number of animals with renal cell tumors and percentage incidence of tumor as compared to the DEN initiated and Fe-NTA promoted rats. The study was further histologically confirmed. These results suggest a potential role of T chebula in protection from Fe-NTA-induced renal carcinogenesis and oxidative damage.