Role of Vitamin E-acetate on Cisplatin induced genotoxicity: An in vivo analysis

Central European Journal of Biology (Impact Factor: 0.82). 01/2012; DOI: 10.2478/s11535-012-0001-z

ABSTRACT Vitamin E has generated immense interest because of its potential of being an antioxidant, a neuroprotector, and a protector against
atherosclerosis, carcinogenesis and cardiovascular disease. However, the prooxidant chemistry of Vitamin E cannot be ignored since
it is related to the generation of peroxyl radicals. In the present study, 125, 250 and 500 mg/kg of Vitamin E-acetate (VE) administered
intraperitoneally (i.p.) to Balb/C mice significantly induced 6.00%, 8.00% and 11.33% (control value=2.33%) of chromosome
aberrations (CA) and 0.88%, 1.39% and 1.81% (control value=0.61%) of micronucleus (MN), following 24 hour of treatment in
the bone marrow cells. In the germ cells, VE did not induce any sperm head abnormality (SHA) after 35 days of exposure. Most
importantly, it has been observed that pre-treatment with VE significantly reduces CA, MN, and SHA induction by chemotherapeutic
drug Cisplatin (CIS). Our findings suggest that lone treatment with VE induce genotoxicity in somatic cells after 24 and 48 hours of
exposure but not in germ cells after 35 days of exposure, whereas pre-treatment with VE reduces CIS induced genotoxicity as well
as cytotoxicity. There exists a thin line of difference on the behavioral transition of VE when acting alone and when acting with a drug.

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    ABSTRACT: OBJECTIVE: To evaluate the evidence of the supplements vitamin C and vitamin E for treatment and prevention of cancer.METHODS: Systematic review of trials and meta-analysis.DATA SOURCES AND MAIN RESULTS: Thirty-eight studies showed scant evidence that vitamin C or vitamin E beneficially affects survival. In the ATBC Cancer Prevention Study Group, no statistically significant effect of treatment was seen for any cancer individually, and our pooled relative risk (regardless of tumor type) for α-tocopherol alone was 0.91 (95% confidence interval [CI]: 0.74, 1.12). All cause mortality was not significant. In the Linxian General Population Trial, the relative risks for cancer death for vitamin C (combined with molybdenum) was 1.06 (95% CI: 0.92, 1.21) and for vitamin E (combined with β-carotene and selenium) was 0.87 (95% CI: 0.76, 1.00). We identified only 3 studies that reported statistically significant beneficial results: vitamin C (in combination with BCG) was found to be beneficial in a single trial of bladder cancer and vitamin E (in combination with ω-3 fatty acid) increased survival in patients with advanced cancer. In the ATBC trial, in analyses of 6 individual cancers, the prevention of prostate cancer in subjects treated with α-tocopherol was statistically significant (RR=0.64, 95% CI: 0.44, 0.94).CONCLUSIONS: The systematic review of the literature does not support the hypothesis that the use of supplements of vitamin C or vitamin E in the doses tested helps prevent and/or treat cancer in the populations tested. There were isolated findings of benefit, which require confirmation.
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    ABSTRACT: Epidemiological and experimental studies suggest that antioxidants like vitamin E (alpha-tocopherol) may play an important role in prevention of chronic disease. Several observational surveys have linked populations with a large intake of vitamin E with reduced incidence of heart disease. These observations have been strengthened by the demonstration of strong antioxidant activity by vitamin E in cellular, molecular and animal experiments. These results have highlighted a potential role for vitamin E supplementation in the prevention of chronic disease in humans. Interestingly however, large-scale clinical trials of vitamin E and other antioxidants in preventing specific disease processes (e.g., coronary artery disease) have generated conflicting and mixed outcomes. In this review, the role of vitamin E in the prevention of atherosclerosis and carcinogenesis has been carefully examined with particular emphasis on salient human studies (clinical trials) and their limitations. In addition, pertinent biochemical, physiological and metabolic features of vitamin E have also been incorporated. A list of common natural food sources of vitamin E has been provided. Important in vitro and animal studies related to the antiatherosclerotic and anticarcinogenic actions of vitamin E have been discussed in detail. Finally, the direction of future investigations in primary and secondary prevention of chronic diseases by vitamin E supplementation has been outlined.
    Journal of the American College of Nutrition 09/2003; 22(4):258-68. · 1.74 Impact Factor
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    ABSTRACT: To evaluate and synthesize the evidence on the effect of supplements of vitamin E on the prevention and treatment of cardiovascular disease. Systematic review of placebo-controlled randomized controlled trials; meta-analysis where justified. Eighty-four eligible trials were identified. For the outcomes of all-cause mortality, cardiovascular mortality, fatal or nonfatal myocardial infarction, and blood lipids, neither supplements of vitamin E alone nor vitamin E given with other agents yielded a statistically significant beneficial or adverse pooled relative risk (for example, pooled relative risk of vitamin E alone = 0.96 [95% confidence interval (CI), 0.84 to 1.10]; 0.97 [95% CI, 0.80 to 1.90]; and 0.72 [95% CI, 0.51 to 1.02] for all-cause mortality, cardiovascular mortality, and nonfatal myocardial infarction, respectively. There is good evidence that vitamin E supplementation does not beneficially or adversely affect cardiovascular outcomes.
    Journal of General Internal Medicine 05/2004; 19(4):380-9. · 3.28 Impact Factor


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May 22, 2014