Seppet E K, Kadaia A I, Kallikorm A P, Saks V A
Biokhimiia. 1990 Jun;55(6):1081-7.
The mechanisms of the phosphocreatine/creatine ratio decrease in female Wistar rats with hyperthyroidism were studied. L-Thyroxin was injected to animals in doses of 50 and 100 micrograms/100 g of body weight, daily for 1 and 2 weeks. Oxidative phosphorylation and the rate of phosphocreatine synthesis were studied in isolated rat heart mitochondria. It was found that hyperthyroidism caused an increase in the ADP-activated mitochondrial respiration, whereas the coupling between electron transport and ADP phosphorylated remained at a constant level. Besides oxidative phosphorylation, activation, hyperthyroidism increased the rate of phosphocreatine synthesis at high values of the phosphocreatine/oxygen ratio. Thus, hyperthyroidism is unaccompanied by and significant changes in the coupling of mitochondrial creatine kinase with oxidative phosphorylation.
研究了甲状腺功能亢进的雌性Wistar大鼠磷酸肌酸/肌酸比率降低的机制。以50和100微克/100克体重的剂量每天给动物注射L-甲状腺素,持续1和2周。在分离的大鼠心脏线粒体中研究了氧化磷酸化和磷酸肌酸合成速率。发现甲状腺功能亢进导致ADP激活的线粒体呼吸增加,而电子传递与ADP磷酸化之间的偶联保持在恒定水平。除了氧化磷酸化激活外,甲状腺功能亢进在磷酸肌酸/氧比率高值时增加了磷酸肌酸合成速率。因此,甲状腺功能亢进并未伴随线粒体肌酸激酶与氧化磷酸化偶联的显著变化。