Asayama K, Dobashi K, Hayashibe H, Megata Y, Kato K
Department of Pediatrics, Yamanashi Medical College, Japan.
Endocrinology. 1987 Dec;121(6):2112-8. doi: 10.1210/endo-121-6-2112.
This study was designed to determine if peroxidation of biomembrane lipid and the protective system can be modified by the change in oxidative metabolism induced by thyroid dysfunction. The free radical scavengers (i.e. cuprozinc cytosolic and mangano mitochondrial superoxide dismutases, glutathione peroxidase, and catalase), mitochondrial oxidative marker enzymes (cytochrome c oxidase and fumarase), and lipid peroxide were measured in liver, heart, soleus (slow oxidative), and extensor digitorum longus (fast glycolytic) muscles. Rats were rendered hyper- or hypothyroid for 4 weeks and then killed. Superoxide dismutases were detected by specific RIAs: catalase by polarography, and lipid peroxide by fluorimetry. Hypothyroid rats failed to grow, while hyperthyroid rats had hypertrophied hearts but no growth failure. An increase in lipid peroxide was observed in the soleus and heart muscles of hyperthyroid rats. This was accompanied by an increase in mitochondrial superoxide dismutase and oxidative markers. No such change was observed in either fast glycolytic muscle or liver. Glutathione peroxidase decreased in all tissues of hyperthyroid rats, and there was a parallel decrease in catalase in most tissues. On the other hand, hypothyroidism induced a reduction in oxidative markers and mitochondrial superoxide dismutase in heart and skeletal muscles, but only a marginal change in lipid peroxidation. The cytosolic superoxide dismutase did not change in relation to either oxidative metabolism or lipid peroxidation. These results suggest that the enhanced oxidative metabolism and decreased glutathione peroxidase in hyperthyroidism result in an increase in lipid peroxidation and, in slow oxidative and heart muscle, possible organ damage. No adverse reaction mediated by active oxygen species was found in hypothyroid rat tissues.
本研究旨在确定甲状腺功能障碍引起的氧化代谢变化是否会改变生物膜脂质的过氧化作用及其保护系统。对肝脏、心脏、比目鱼肌（慢氧化型）和趾长伸肌（快糖酵解型）中的自由基清除剂（即铜锌胞质超氧化物歧化酶、锰线粒体超氧化物歧化酶、谷胱甘肽过氧化物酶和过氧化氢酶）、线粒体氧化标记酶（细胞色素c氧化酶和延胡索酸酶）以及脂质过氧化物进行了测定。将大鼠造成甲状腺功能亢进或减退状态4周，然后处死。通过特异性放射免疫分析法检测超氧化物歧化酶，通过极谱法检测过氧化氢酶，通过荧光法检测脂质过氧化物。甲状腺功能减退的大鼠生长停滞，而甲状腺功能亢进的大鼠心脏肥大但无生长障碍。在甲状腺功能亢进大鼠的比目鱼肌和心肌中观察到脂质过氧化物增加。同时线粒体超氧化物歧化酶和氧化标记物也增加。在快糖酵解型肌肉或肝脏中未观察到此类变化。甲状腺功能亢进大鼠所有组织中的谷胱甘肽过氧化物酶均降低，大多数组织中的过氧化氢酶也相应降低。另一方面，甲状腺功能减退导致心脏和骨骼肌中的氧化标记物和线粒体超氧化物歧化酶减少，但脂质过氧化仅发生轻微变化。胞质超氧化物歧化酶与氧化代谢或脂质过氧化均无关联。这些结果表明，甲状腺功能亢进时氧化代谢增强和谷胱甘肽过氧化物酶减少导致脂质过氧化增加，在慢氧化型肌肉和心肌中可能造成器官损伤。在甲状腺功能减退大鼠组织中未发现由活性氧介导的不良反应。
