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.
Prasad
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Section of Chemoprevention and Nutrition Toxicology, Department of Medical Elementology and Toxicology, Jamia Hamdard (Hamdard University), Hamdard Nagar, New Delhi, India.
Khan
T H
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Jahangir
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Sultana
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D000818:Animals; D016588:Anticarcinogenic Agents / Q000494:pharmacology*; D000975:Antioxidants / Q000378:metabolism / Q000494:pharmacology*; D002273:Carcinogens / Q000633:toxicity*; D049109:Cell Proliferation / Q000187:drug effects*; D002614:Chelating Agents / Q000633:toxicity*; D004247:DNA / Q000096:biosynthesis / Q000235:genetics; D005290:Ferric Compounds / Q000633:toxicity*; D005978:Glutathione / Q000378:metabolism; D007668:Kidney / Q000166:cytology* / Q000187:drug effects / Q000201:enzymology; D007674:Kidney Diseases / Q000139:chemically induced / Q000517:prevention & control; D007677:Kidney Function Tests; D007680:Kidney Neoplasms / Q000139:chemically induced / Q000517:prevention & control; D015227:Lipid Peroxidation / Q000187:drug effects; D008297:Male; D008861:Microsomes / Q000187:drug effects / Q000378:metabolism; D009571:Nitrilotriacetic Acid / Q000031:analogs & derivatives* / Q000633:toxicity; D018384:Oxidative Stress / Q000187:drug effects*; D010936:Plant Extracts / Q000737:chemistry / Q000494:pharmacology; D011808:Quinone Reductases / Q000378:metabolism; D051381:Rats; D017208:Rats, Wistar; D029766:Terminalia / Q000737:chemistry*; D014969:Xanthine Oxidase / Q000378:metabolism
D016588:Anticarcinogenic Agents; D000975:Antioxidants; D002273:Carcinogens; D002614:Chelating Agents; D005290:Ferric Compounds; D010936:Plant Extracts; D004247:DNA; D014969:Xanthine Oxidase; D011808:Quinone Reductases; D005978:Glutathione; D009571:Nitrilotriacetic Acid; C020326:ferric nitrilotriacetate