Suppr超能文献

链脲佐菌素诱导糖尿病急性期大鼠心脏线粒体膜重塑中的内源性保护机制

Endogenous protective mechanisms in remodeling of rat heart mitochondrial membranes in the acute phase of streptozotocin-induced diabetes.

作者信息

Ferko M, Habodászová D, Waczulíková I, Mujkošová J, Kucharská J, Šikurová L, Ziegelhoffer B, Styk J, Ziegelhoffer A

机构信息

Institute for Heart Research, Centre of Excellence in Cardiovascular Sciences, Slovak Academy of Sciences, Bratislava, Slovakia.

出版信息

Physiol Res. 2008;57 Suppl 2:S67-S73. doi: 10.33549/physiolres.931554. Epub 2008 Mar 28.

Abstract

The aim of present study was to investigate functional and physical alterations in membranes of heart mitochondria that are associated with remodeling of these organelles in acute phase of streptozotocin-induced diabetes and to elucidate the role of these changes in adaptation of the heart to acute streptozotocin-induced diabetes (evaluated 8 days after single dose streptozotocin application to male Wistar rats). Action of free radicals on the respiratory chain of diabetic-heart mitochondria was manifested by 17 % increase (p<0.05) in oxidized form of the coenzyme Q(10) and resulted in a decrease of states S3 and S4 respiration, the respiratory control index, rate of phosphorylation (all p<0.01) and the mitochondrial transmembrane potential (p<0.05), but the ADP/O ratio decreased only moderately (p>0.05). On the contrary, membrane fluidity and the total mitochondrial Mg2+-ATPase activity increased (both p<0.05). In diabetic heart mitochondria, linear regression analysis revealed a reciprocal relationship between the increase in membrane fluidity and decrease in trans-membrane potential (p<0.05, r = 0.67). Changes in membrane fluidity, transmembrane potential, Mg2+-ATPase activity and the almost preserved ADP/O ratio appear as the manifestation of endogenous protective mechanisms participating in the functional remodeling of mitochondria which contributes to adaptation of the heart to diabetes.

摘要

本研究的目的是调查链脲佐菌素诱导的糖尿病急性期心脏线粒体膜的功能和物理改变,这些改变与这些细胞器的重塑有关,并阐明这些变化在心脏适应急性链脲佐菌素诱导的糖尿病中的作用(在雄性Wistar大鼠单次注射链脲佐菌素8天后进行评估)。自由基对糖尿病心脏线粒体呼吸链的作用表现为辅酶Q(10)氧化形式增加17%(p<0.05),并导致状态S3和S4呼吸、呼吸控制指数、磷酸化速率(均p<0.01)和线粒体跨膜电位(p<0.05)降低,但ADP/O比值仅适度降低(p>0.05)。相反,膜流动性和线粒体总Mg2+-ATP酶活性增加(均p<0.05)。在糖尿病心脏线粒体中,线性回归分析显示膜流动性增加与跨膜电位降低之间呈负相关(p<0.05,r = 0.67)。膜流动性、跨膜电位、Mg2+-ATP酶活性的变化以及几乎保持不变的ADP/O比值似乎是参与线粒体功能重塑的内源性保护机制的表现,这有助于心脏适应糖尿病。

文献AI研究员

20分钟写一篇综述,助力文献阅读效率提升50倍。

立即体验

用中文搜PubMed

大模型驱动的PubMed中文搜索引擎

马上搜索

文档翻译

学术文献翻译模型,支持多种主流文档格式。

立即体验