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[实验性甲状旁腺功能减退症中线粒体的功能活性]

[Functional activity of mitochondria in experimental hypoparathyroidism].

作者信息

Ovsepian R S, Ter-Markosian A S, Khudaverdian D N

出版信息

Probl Endokrinol (Mosk). 1981 Sep-Oct;27(5):75-9.

PMID:6270650
Abstract

Respiration and oxidative phosphorylation of the brain and hepatic mitochondria, as well as the activity of succinate dehydrogenase, succinate-cytochrome-c-reductase and cytochrome oxydase were studied in experimental hypoparathyrosis. Activated respiration and decreased effectiveness of the brain and hepatic mitochondrial phosphorylation and enhanced succinate dehydrogenase activity are seen during hypoparathyrosis development. It is suggested that alterations in mitochondrial functional activity are caused not only by the changed blood calcium ion number, but also by hypoxia, developing in experimental hypoparathyrosis.

摘要

在实验性甲状旁腺功能减退症中,对脑和肝线粒体的呼吸作用、氧化磷酸化以及琥珀酸脱氢酶、琥珀酸 - 细胞色素c还原酶和细胞色素氧化酶的活性进行了研究。在甲状旁腺功能减退症发展过程中,可见脑和肝线粒体的呼吸作用增强、磷酸化效率降低以及琥珀酸脱氢酶活性增强。提示线粒体功能活性的改变不仅是由血钙离子数量变化引起的,还与实验性甲状旁腺功能减退症中发生的缺氧有关。

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