Chemomodulatory effect of Ficus racemosa extract against chemically induced renal carcinogenesis and oxidative damage response in Wistar rats.
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, gamma-glutamyl transpeptidase and hydrogen peroxide (H(2)O(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 [(3)H] 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 gamma-glutamyl transpeptidase, lipid peroxidation, xanthine oxidase, H(2)O(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.
Khan
Naghma
N
Section of Chemoprevention and Nutrition Toxicology, Department of Medical Elementology and Toxicology, Faculty of Science, Jamia Hamdard (Hamdard University), New Delhi 110 062, India.
Sultana
Sarwat
S
D000818:Animals; D001806:Blood Urea Nitrogen; D002374:Catalase / Q000378:metabolism; D002614:Chelating Agents / Q000633:toxicity; D002851:Chromatography, High Pressure Liquid; D002855:Chromatography, Thin Layer; D003404:Creatinine / Q000097:blood; D004247:DNA / Q000096:biosynthesis; D004052:Diethylnitrosamine; D005260:Female; D030681:Ficus / Q000737:chemistry*; D005978:Glutathione / Q000378:metabolism; D006861:Hydrogen Peroxide / Q000378:metabolism; D007680:Kidney Neoplasms / Q000139:chemically induced* / Q000517:prevention & control*; D015227:Lipid Peroxidation / Q000187:drug effects; D008861:Microsomes / Q000187:drug effects / Q000378:metabolism; D016660:NAD(P)H Dehydrogenase (Quinone) / Q000378:metabolism; D009571:Nitrilotriacetic Acid / Q000633:toxicity; D009955:Ornithine Decarboxylase / Q000378:metabolism; D018384:Oxidative Stress / Q000187:drug effects*; D010936:Plant Extracts / Q000737:chemistry / Q000627:therapeutic use; D051381:Rats; D017208:Rats, Wistar; D013936:Thymidine / Q000378:metabolism; D014466:Ultraviolet Rays; D014969:Xanthine Oxidase / Q000378:metabolism; D005723:gamma-Glutamyltransferase / Q000378:metabolism
D002614:Chelating Agents; D010936:Plant Extracts; D004052:Diethylnitrosamine; D004247:DNA; D003404:Creatinine; D006861:Hydrogen Peroxide; D002374:Catalase; D014969:Xanthine Oxidase; D016660:NAD(P)H Dehydrogenase (Quinone); D005723:gamma-Glutamyltransferase; D009955:Ornithine Decarboxylase; D005978:Glutathione; D009571:Nitrilotriacetic Acid; D013936:Thymidine