| pubmed-article:2897437 | pubmed:abstractText | In four experiments, attempts were made to induce nutritional myopathy in calves given a selenium- and vitamin E-deficient diet (less than 0.01 mg Se/kg, less than 2 mg total vitamin E/kg). In housed calves, combined selenium and vitamin E deficiency was insufficient to provoke the large increase in plasma creatine kinase activity typical of muscle damage. Such increases were only obtained when selenium- and vitamin E-deficient calves were turned out from indoor housing in small pens to open pasture. The rises in plasma creatine kinase activity on turnout were prevented when the calves had consumed diets supplemented with 0.1 mg Se/kg (as Na2SeO3). The percentage of the polyunsaturated fatty acid, linolenic acid (18:3 omega 3), in plasma total fatty acids was up to 10-fold higher in calves consuming fresh grass at pasture or indoors than in those housed indoors and fed purified diet. However, in the housed calves there were no rises in plasma creatine kinase activity, whereas large increases occurred in those turned out to pasture. Thus, because increased dietary polyunsaturated fatty acid at turnout is not the sole trigger for the development of myopathy in selenium- and vitamin E-deficient calves, additional unidentified dietary or environmental factors must also be involved. | lld:pubmed |
