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甲状腺功能减退使肝脏线粒体对膜通透性转换孔的开放产生抗性。

Hypothyroidism renders liver mitochondria resistant to the opening of membrane permeability transition pore.

作者信息

Chávez E, Franco M, Reyes-Vivas H, Zazueta C, Ramírez J, Carrillo R

机构信息

Departamento de Bioquímica, Instituto Nacional de Cardiología, Ignacio Chávez, México, D.F., Mexico.

出版信息

Biochim Biophys Acta. 1998 Sep 30;1407(3):243-8. doi: 10.1016/s0925-4439(98)00048-9.

DOI:10.1016/s0925-4439(98)00048-9
PMID:9748606
Abstract

Membrane permeability was examined in liver mitochondria isolated from hypothyroid rats. It was found that such a thyroid status provides substantial protection from membrane leakiness as induced by Ca2+ loading. Thus, these mitochondria are less prone to undergoing permeability transition than mitochondria from euthyroid rats. The above conclusion was reached on the basis of the following two facts: (1) hypothyroid mitochondria are not strictly dependent on the addition of ADP to retain high matrix Ca2+ concentrations, and (2) carboxyatractyloside, antimycin A or carbonyl cyanide-m-chlorophenyl hydrazone failed to promote Ca2+ efflux. We discuss the possible relevance of the low content of membrane cardiolipin as well as the low expression of the adenine nucleotide translocase as responsible for the resistance to membrane damage.

摘要

对从甲状腺功能减退大鼠分离出的肝脏线粒体的膜通透性进行了检测。结果发现,这种甲状腺状态能为线粒体提供显著保护,使其免受钙离子负载诱导的膜渗漏影响。因此,与甲状腺功能正常大鼠的线粒体相比,这些线粒体发生通透性转变的倾向较小。上述结论基于以下两个事实得出:(1)甲状腺功能减退的线粒体并非严格依赖添加二磷酸腺苷(ADP)来维持高浓度的基质钙离子,(2)羧基苍术苷、抗霉素A或羰基氰化物-间氯苯腙均无法促进钙离子外流。我们讨论了膜心磷脂含量低以及腺嘌呤核苷酸转位酶表达低可能与抗膜损伤作用的相关性。

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