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Gender-dependence of hyperthermia-induced changes in respiration of rat liver mitochondria

机译:热疗诱导的大鼠肝线粒体呼吸变化的性别依赖性

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摘要

The effect of hyperthermia on the respiration of liver mitochondria derived from animals of different genders was estimated. We compared the effect of heating in the febrile (40 °C) and supraphysiological (41-46 °C) temperature range on the respiration rate in metabolic state 2 (V_2) and state 3 (V_3) of isolated mitochondria derived from male and female rat liver. Our results indicate that an increase of temperature in the fever range activates female but inhibits male liver mitochondrial respiration in state 3. Female mitochondria are less sensitive to supraphysiological temperature hyperthermia (41-43 °C). However, a severe hyperthermia (44-46 °C) strongly inhibits and uncouples oxidative phosphorylation in mitochondria, but the temperatureinduced increase in inner membrane permeability is stronger in female mitochondria. At 46 °C, independently of gender, mitochondria are completely uncoupled (V_2 = V_3) and are unable to phosphorylate ADP. The increased respiration rate in the uncoupled state proves that febrile temperature (40 °C) activates oxidation processes in liver mitochondria isolated from female rats. For this reason, at 40 °C the respiratory control index (RCI) decreases to a much lower extent in mitochondria derived from female liver.
机译:估计了高温对源自不同性别动物的肝线粒体呼吸的影响。我们比较了发热(40°C)和超生理温度(41-46°C)加热对男性和女性分离的线粒体代谢状态2(V_2)和状态3(V_3)呼吸速率的影响大鼠肝脏。我们的结果表明,发烧范围内温度的升高会在状态3中激活雌性,但抑制雄性肝线粒体呼吸。雌性线粒体对超生理温度过高敏感性(41-43°C)较不敏感。但是,严重的体温过高(44-46°C)会强烈抑制并解耦线粒体中的氧化磷酸化,但温度诱导的雌性线粒体内膜渗透性增加更强。在46°C下,无论性别,线粒体都完全不偶联(V_2 = V_3),并且无法磷酸化ADP。在非耦合状态下增加的呼吸速率证明,发热温度(40°C)激活了从雌性大鼠分离的肝线粒体中的氧化过程。因此,在40°C时,源自女性肝脏的线粒体中的呼吸控制指数(RCI)降低到非常低的程度。

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