Nishiki K, Erecińska M, Wilson D F, Cooper S
Am J Physiol. 1978 Nov;235(5):C212-9. doi: 10.1152/ajpcell.1978.235.5.C212.
The energy relationships between cytosolic and mitochondrial metabolism were studied in the hearts from euthyroid, hypothyroid, and hyperthyroid rats. Isolated mitochondria showed high respiratory control ratios and impermeability to exogenous NADH. Hypo- and hyperthyroidism, respectively, resulted in lower and higher contents of both cytochromes per mitochondrion and mitochondrial protein per gram of wet weight of heart without changes in the ratio of cytochrome c to cytochrome aa3. In isolated perfused heart, the hyperthyroid state led to an increase in work rate and thereby an elevation of Vo2, which resulted in an increase oxidation-reduction turnover number for the cytochromes. An agreement was found between [ATP]/[ADP][Pi] of cytosolic free adenine nucleotides and the value calculated from a mathematical model of mitochondrial respiration. This implies that mitochondrial respiration is controlled at the cytochrome oxidase reaction and that oxidative phosphorylation in intact tissue is tightly coupled irrespective of thyroid state. It is concluded that thyroid hormone causes an increase in the mitochondrial mass, mitochondrial cytochrome content, and respiratory rate, and consequently expands the capacity of oxidative metabolism without an uncoupling effect on oxidative phosphorylation.
研究了正常甲状腺、甲状腺功能减退和甲状腺功能亢进大鼠心脏中胞质和线粒体代谢之间的能量关系。分离的线粒体显示出高呼吸控制率且对外源NADH不渗透。甲状腺功能减退和亢进分别导致每个线粒体中细胞色素含量以及每克心脏湿重中线粒体蛋白含量降低和升高，而细胞色素c与细胞色素aa3的比例没有变化。在离体灌注心脏中，甲状腺功能亢进状态导致工作率增加，从而使Vo2升高，这导致细胞色素的氧化还原周转数增加。发现胞质游离腺嘌呤核苷酸的[ATP]/[ADP][Pi]与根据线粒体呼吸数学模型计算的值之间存在一致性。这意味着线粒体呼吸在细胞色素氧化酶反应处受到控制，并且完整组织中的氧化磷酸化紧密偶联，与甲状腺状态无关。得出的结论是，甲状腺激素会导致线粒体质量、线粒体细胞色素含量和呼吸速率增加，从而扩大氧化代谢能力，而不会对氧化磷酸化产生解偶联作用。
