α-Tocopherol prevents lymphoma by improving antioxidant defence system of mice.
Increased level of ROS causes oxidative stress and leads to various pathological conditions including cancer. Therefore antioxidants should contribute to cancer prevention by improving antioxidant defense system and thereby protecting the cell from oxidative damage. In the present study we have validated the hypothesis by evaluating the antioxidant action of α-tocopherol. The effect of α-tocopherol is analyzed on oxidative stress as well as its regulation on antioxidant defense system. Oxidative stress is measured in terms of reduced glutathione and protein carbonylation. To evaluate the role of α-tocopherol on antioxidant defense system, the activities and expressions of antioxidant enzymes like glutathione peroxidase, catalase and superoxide dismutase are analyzed by activity gel assay and by RT-PCR respectively. These enzyme activities and/or expressions are found to be improved by α-tocopherol in lymphoma bearing mice which brings down the oxidative stress as reflected by increased level of reduced glutathione as well as decreased protein carbonylation. The effect of α-tocopherol is further analyzed on general characteristics of lymphoma growth like body weight, longevity, accumulation of ascites fluid, angiogenesis in peritoneum, morphology of liver and abundance of lymphocytes. The antioxidant α-tocopherol is found to check lymphoma growth. The results suggest that α-tocopherol contributes to lymphoma prevention by improving antioxidant defence system of mice.
Biochemistry & Molecular Biology Laboratory, Centre of Advanced Study in Zoology, Banaras Hindu University, Varanasi, India.
Renu
R
Sharma
Manjula
M
Vinayak
D000818:Animals; D000970:Antineoplastic Agents / Q000494:pharmacology*; D000975:Antioxidants / Q000378:metabolism*; D001202:Ascitic Fluid / Q000473:pathology; D002374:Catalase / Q000378:metabolism; D005978:Glutathione / Q000378:metabolism; D005979:Glutathione Peroxidase / Q000378:metabolism; D008099:Liver / Q000187:drug effects / Q000201:enzymology; D018655:Lymphocyte Count; D008223:Lymphoma / Q000473:pathology / Q000517:prevention & control*; D008297:Male; D051379:Mice; D008806:Mice, Inbred AKR; D018384:Oxidative Stress / Q000187:drug effects; D050050:Protein Carbonylation / Q000187:drug effects; D013482:Superoxide Dismutase / Q000378:metabolism; D047368:Tumor Burden / Q000187:drug effects; D023041:Xenograft Model Antitumor Assays; D024502:alpha-Tocopherol / Q000494:pharmacology*; D000094765:Glutathione Peroxidase GPX1
D000970:Antineoplastic Agents; D000975:Antioxidants; D002374:Catalase; D005979:Glutathione Peroxidase; D013482:Superoxide Dismutase; D005978:Glutathione; D024502:alpha-Tocopherol; D000094765:Glutathione Peroxidase GPX1; C000722068:Gpx1 protein, mouse