Permeability transition was examined in heart mitochondria isolated from neonate rats. We found that these mitochondria were more susceptible to Ca(2+)-induced membrane leakiness than mitochondria from adult rats. In K(+) containing medium, at 25 °C, mitochondria were unable to accumulate Ca(2+). Conversely, in Na(+) containing medium, mitochondria accumulated effectively Ca(2+). At 15 °C mitochondria accumulated Ca(2+) regardless of the presence of K(+). Kinetics of Ca(2+) accumulation showed a similar Vmax as that of adult mitochondria. Lipid milieu of inner membrane contained more unsaturated fatty acids than adult mitochondria. Aconitase inhibition and high thiobarbituric acid-reactive substances (TBARS) indicate that oxidative stress caused mitochondrial damage. In addition, proteomics analysis showed that there is a considerable diminution of succinate dehydrogenase C and subunit 4 of cytochrome oxidase in neonate mitochondria. Our proposal is that dysfunction of the respiratory chain makes neonate mitochondria more susceptible to damage by oxidative stress.

中文翻译：

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关于钙诱导的新生儿心脏线粒体通透性转变的特性。

在从新生大鼠分离的心脏线粒体中检查渗透性转变。我们发现这些线粒体比成年大鼠的线粒体更容易受到 Ca(2+) 诱导的膜渗漏。在含 K(+) 的培养基中，在 25 °C 时，线粒体无法积累 Ca(2+)。相反，在含有 Na(+) 的培养基中，线粒体有效地积累了 Ca(2+)。在 15 °C 线粒体积累 Ca(2+) 不管 K(+) 的存在。Ca(2+) 积累的动力学表现出与成人线粒体相似的Vmax。内膜的脂质环境比成人线粒体含有更多的不饱和脂肪酸。乌头酸酶抑制和高硫代巴比妥酸反应性物质 (TBARS) 表明氧化应激导致线粒体损伤。此外，蛋白质组学分析表明，新生儿线粒体中琥珀酸脱氢酶C和细胞色素氧化酶亚基4显着减少。我们的建议是呼吸链功能障碍使新生儿线粒体更容易受到氧化应激的损害。