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Chemomodulatory effect ofFicus racemosaextract against chemically induced renal carcinogenesis and oxidative damage response in Wistar rats

Life Sciences
Publication Date
DOI: 10.1016/j.lfs.2004.12.041
  • Carcinogenesis
  • Chemoprevention
  • Ferric Nitrilotriacetate
  • Ficus Racemosaextract
  • Oxidative Stress
  • Biology
  • Communication


Abstract Ferric nitrilotriacetate (Fe-NTA) is a well-known renal carcinogen. In this communication, we show the chemopreventive effect of Ficus racemosa extract against Fe-NTA-induced renal oxidative stress, hyperproliferative response and renal carcinogenesis in rats. Fe-NTA (9 mg Fe/kg body weight, intraperitoneally) enhances renal lipid peroxidation, xanthine oxidase, γ-glutamyl transpeptidase and hydrogen peroxide (H 2O 2) generation with reduction in renal glutathione content, antioxidant enzymes, viz., glutathione peroxidase, glutathione reductase, catalase, glucose-6-phosphate dehydrogenase and phase-II metabolising enzymes such as glutathione- S-transferase and quinone reductase. It also enhances blood urea nitrogen, serum creatinine, ornithine decarboxylase (ODC) activity and thymidine [ 3H] incorporation into renal DNA. It also enhances DEN ( N-diethylnitrosamine) initiated renal carcinogenesis by increasing the percentage incidence of tumors. Treatment of rats orally with F. racemosa extract (200 and 400 mg/kg body weight) resulted in significant decrease in γ-glutamyl transpeptidase, lipid peroxidation, xanthine oxidase, H 2O 2 generation, blood urea nitrogen, serum creatinine, renal ODC activity, DNA synthesis ( P < 0.001) and incidence of tumors. Renal glutathione content ( P < 0.01), glutathione metabolizing enzymes ( P < 0.001) and antioxidant enzymes were also recovered to significant level ( P < 0.001). Thus, our data suggests that F. racemosa extract is a potent chemopreventive agent and suppresses Fe-NTA-induced renal carcinogenesis and oxidative damage response in Wistar rats.

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