Asayama K, Dobashi K, Hayashibe H, Kato K
Department of Pediatrics, Yamanashi Medical College, Japan.
J Nutr Sci Vitaminol (Tokyo). 1989 Oct;35(5):407-18. doi: 10.3177/jnsv.35.407.
To determine whether vitamin E protects against thyroxine-induced oxidative stress in heart and soleus (slow oxidative) muscles, lipid peroxide (thiobarbituric acid-reactive substances) and antioxidant enzymes were measured in those tissues of hyperthyroid rats supplemented with vitamin E. The rats were rendered hyperthyroid by the administration of L-thyroxine in their drinking water. In experiment (EXPT) I, 30 mg/kg/dose of alpha-tocopheryl acetate was administered to the vitamin E-treated group. In EXPT II, the rats were fed a diet containing either less than 1 IU/kg (deficient diet), 20 IU/kg (control E diet), or 500 IU/kg (high E diet) of vitamin E and hyperthyroidism was induced. In EXPT I, hyperthyroidism induced an increase in oxidative enzymes, mitochondrial superoxide dismutase and lipid peroxide level, and a decrease in cytosolic superoxide dismutase, glutathione peroxidase and catalase in both tissues. Vitamin E treatment inhibited the increase in lipid peroxide level totally in the heart and partially in the soleus, with minimal changes in the other biochemical indices studied. In EXPT II, the lipid peroxide level was markedly increased in both tissues of the vitamin E-deficient group, and decreased in those of the group fed high E diet. There were some adaptive changes in the levels of cytosolic superoxide dismutase, glutathione peroxidase, and catalase in response to vitamin E deficiency, whereas neither oxidative enzymes nor mitochondrial superoxide dismutase were altered. These results suggest that vitamin E protects against lipid peroxidation in hyperthyroid heart and skeletal muscle independently of the changes in oxidative enzymes and antioxidant enzymes.
为了确定维生素E是否能保护心脏和比目鱼肌（慢氧化型）免受甲状腺素诱导的氧化应激影响，我们检测了补充维生素E的甲状腺功能亢进大鼠这些组织中的脂质过氧化物（硫代巴比妥酸反应性物质）和抗氧化酶。通过在饮用水中添加L-甲状腺素使大鼠甲状腺功能亢进。在实验I中，给维生素E处理组给予30mg/kg/剂量的α-生育酚醋酸酯。在实验II中，给大鼠喂食含维生素E量分别低于1IU/kg（缺乏饮食）、20IU/kg（对照E饮食）或500IU/kg（高E饮食）的饲料并诱导甲状腺功能亢进。在实验I中，甲状腺功能亢进导致两种组织中的氧化酶、线粒体超氧化物歧化酶和脂质过氧化物水平升高，而胞质超氧化物歧化酶、谷胱甘肽过氧化物酶和过氧化氢酶水平降低。维生素E处理完全抑制了心脏中脂质过氧化物水平的升高，对比目鱼肌的抑制作用部分存在，而所研究的其他生化指标变化极小。在实验II中，维生素E缺乏组的两种组织中脂质过氧化物水平显著升高，而高E饮食组的则降低。胞质超氧化物歧化酶、谷胱甘肽过氧化物酶和过氧化氢酶水平因维生素E缺乏而有一些适应性变化，而氧化酶和线粒体超氧化物歧化酶均未改变。这些结果表明，维生素E可独立于氧化酶和抗氧化酶的变化，保护甲状腺功能亢进的心脏和骨骼肌免受脂质过氧化损伤。
