Sterling K
Endocrinology. 1986 Jul;119(1):292-5. doi: 10.1210/endo-119-1-292.
A presumptive mitochondrial T3 receptor previously reported from this and other laboratories appears capable of accounting for the activation of liver mitochondrial oxidative phosphorylation within 30 min after iv bolus injection of nanogram doses of T3 into hypothyroid rats. The inner mitochondrial membrane carrier adenine nucleotide translocase (AdNT) catalyzes the exchange between the extra- and intramitochondrial ADP and ATP, and has been shown by measurements of flux control coefficients to exert a significant measure of control over the rate of mitochondrial oxidative phosphorylation. The activity of this carrier had been reported to be depressed below normal in hypothyroid rats and restored to normal by hormone replacement. Preparations of AdNT from beef heart mitochondria were found to exhibit high affinity, low capacity binding of [125I]T3. The findings make the mitochondrial carrier AdNT a strong candidate for the initiating site for thyroid hormone stimulation in mammalian species.
此前在本实验室及其他实验室报道过的一种推测性线粒体T3受体，似乎能够解释在给甲状腺功能减退的大鼠静脉推注纳克剂量的T3后30分钟内肝脏线粒体氧化磷酸化的激活情况。线粒体内膜载体腺嘌呤核苷酸转位酶（AdNT）催化线粒体外和线粒体内ADP与ATP的交换，并且通过通量控制系数的测量表明，它对线粒体氧化磷酸化速率具有显著的控制作用。据报道，该载体的活性在甲状腺功能减退的大鼠中低于正常水平，并通过激素替代恢复到正常水平。从牛心线粒体中制备的AdNT表现出对[125I]T3的高亲和力、低容量结合。这些发现使线粒体载体AdNT成为哺乳动物物种中甲状腺激素刺激起始位点的有力候选者。
