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This study revealed the occurrence of vitamin E deficiency in the myocardium of 60-day-old Syrian cardiomyopathic hamsters (BIO14.6), and that this deficiency might be related to the increase in lipid peroxide. Vitamin E administration for ten days effectively restored creatininekinase activity and decreased the lipid peroxide content in the myocardium, returning these to normal control levels (F1b). These results indicate that vitamin E deficiency, possibly combined with oxidative stress in the early cardiomyopathic stage plays an important role in initiating the pathogenesis of myocardial lesions.
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