Diehl J F
Z Ernahrungswiss. 1986 Jun;25(2):103-13. doi: 10.1007/BF02020740.
Previous studies of metabolic changes in vitamin E-deficient animals were often difficult to interpret because the vitamin E-free, high PUFA diets used in such studies may have contained high levels of peroxides. Presumed effects of vitamin E deficiency could have been effects of peroxide consumption. Addition of the non-absorbable polymeric antioxidant Anoxomer to a semisynthetic vitamin E-free diet containing cod liver oil was found to suppress peroxide formation. Nevertheless, this diet produced necrotizing myopathy, characterized by high urinary creatine excretion, muscular weakness, and increased rate of incorporation of [1-14C] glycine into muscle proteins. These effects were prevented by vitamin E supplementation. The increased rate of muscle protein turnover is obviously the result of vitamin E deficiency, not the result of consumption of dietary peroxides.
以往对维生素E缺乏动物代谢变化的研究往往难以解释,因为此类研究中使用的不含维生素E、富含多不饱和脂肪酸的饮食可能含有高水平的过氧化物。维生素E缺乏的假定影响可能是过氧化物消耗的影响。研究发现,在含有鱼肝油的半合成无维生素E饮食中添加不可吸收的聚合物抗氧化剂Anoxomer可抑制过氧化物的形成。然而,这种饮食导致了坏死性肌病,其特征是尿肌酸排泄量高、肌肉无力以及[1-14C]甘氨酸掺入肌肉蛋白的速率增加。补充维生素E可预防这些影响。肌肉蛋白质更新率的增加显然是维生素E缺乏的结果,而不是膳食过氧化物消耗的结果。