Swaroop A, Ramasarma T
Biochem J. 1985 Mar 1;226(2):403-8. doi: 10.1042/bj2260403.
Exposure of rats to heat (39 +/- 1 degree C) decreased H2O2 generation in mitochondria of the liver, but not of the kidney or the heart. The effect was obtained with three substrates, succinate, glycerol 1-phosphate and choline, with a decrease to 50% in the first 2-3 days of exposure, and a further decrease on longer exposure. The dehydrogenase activity with only glycerol 1-phosphate decreased, which is indicative of the hypothyroid condition, whereas choline dehydrogenase activity remained unchanged and that of succinate dehydrogenase decreased on long exposure. The serum concentration of thyroxine decreased in heat-exposed rats. Thyroxine treatment of rats increased H2O2 generation. Hypothyroid conditions obtained by treatment with propylthiouracil or thyroidectomy caused a decrease in H2O2 generation and changes in dehydrogenase activities similar to those with heat exposure. Treatment of heat-exposed or thyroidectomized rats with thyroxine stimulated H2O2 generation by a mechanism apparently involving fresh protein synthesis. The results indicate that H2O2 generation in mitochondria of heat-exposed animals is determined by thyroid status.
将大鼠暴露于高温（39±1摄氏度）下，会使肝脏线粒体中的过氧化氢生成量减少，但肾脏和心脏线粒体中的过氧化氢生成量不受影响。使用三种底物（琥珀酸、磷酸甘油和胆碱）时均出现了这种效应，在暴露的头2 - 3天内减少至50%，长时间暴露后进一步减少。仅磷酸甘油的脱氢酶活性降低，这表明甲状腺功能减退，而胆碱脱氢酶活性保持不变，琥珀酸脱氢酶活性在长时间暴露后降低。暴露于高温下的大鼠血清甲状腺素浓度降低。用甲状腺素处理大鼠会增加过氧化氢的生成。用丙基硫氧嘧啶治疗或进行甲状腺切除术导致的甲状腺功能减退会使过氧化氢生成减少，且脱氢酶活性发生与高温暴露类似的变化。用甲状腺素处理高温暴露或甲状腺切除的大鼠会通过一种显然涉及新蛋白质合成的机制刺激过氧化氢的生成。结果表明，高温暴露动物线粒体中的过氧化氢生成由甲状腺状态决定。
