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首页> 外文期刊>Physiological Research >Endogenous Protective Mechanisms in Remodeling of Rat Heart Mitochondrial Membranes in the Acute Phase of Streptozotocin-Induced Diabetes
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Endogenous Protective Mechanisms in Remodeling of Rat Heart Mitochondrial Membranes in the Acute Phase of Streptozotocin-Induced Diabetes

机译:链脲佐菌素诱导的糖尿病急性期大鼠心脏线粒体膜重塑的内源性保护机制。

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摘要

The aim of present study was to investigate functional andphysical alterations in membranes of heart mitochondria that areassociated with remodeling of these organelles in acute phase ofstreptozotocin-induced diabetes and to elucidate the role of thesechanges in adaptation of the heart to acute streptozotocin-induced diabetes (evaluated 8 days after single dosestreptozotocin application to male Wistar rats). Action of freeradicals on the respiratory chain of diabetic-heart mitochondriawas manifested by 17 % increase (p<0.05) in oxidized form ofthe coenzyme Q_(10)and resulted in a decrease of states S3 andS4respiration, 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 totalmitochondrial Mg~(2+)-ATPase activity increased (both p<0.05). Indiabetic heart mitochondria, linear regression analysis revealed areciprocal relationship between the increase in membrane fluidityand decrease in trans-membrane potential (p<0.05, r = 0.67).Changes in membrane fluidity, transmembrane potential, Mg~(2+)-ATPase activity and the almost preserved ADP/O ratio appear asthe manifestation of endogenous protective mechanismsparticipating in the functional remodeling of mitochondria whichcontributes to adaptation of the heart to diabetes.
机译:本研究的目的是研究在链脲佐菌素诱导的糖尿病急性期与这些细胞器重塑相关的区域线粒体膜的功能和物理改变,并阐明这些改变在心脏适应急性链脲佐菌素诱导的糖尿病中的作用(评估对雄性Wistar大鼠单剂量应用链脲佐菌素后8天。自由基对糖尿病性心脏线粒体呼吸链的作用表现为辅酶Q_(10)的氧化形式增加了17%(p <0.05),并导致状态S3和S4呼吸,呼吸控制指数,磷酸化率降低(所有p <0.01)和线粒体跨膜电位(p <0.05),但ADP / O比仅适度下降(p> 0.05)。相反,膜流动性和总线粒体Mg〜(2 +)-ATPase活性增加(均p <0.05)。印度心脏线粒体的线性回归分析显示膜流动性的增加与跨膜电位的下降呈正相关(p <0.05,r = 0.67)。膜流动性,跨膜电位,Mg〜(2 +)-ATPase活性和几乎保持不变的ADP / O比表现为参与线粒体功能重构的内源性保护机制的表现,这有助于心脏适应糖尿病。

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