ATP合酶对心脏线粒体中Ca2+呼吸刺激的贡献。

R Baniene, Z Nauciene, S Maslauskaite, G Baliutyte, V Mildaziene
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引用次数: 8

摘要

采用多种实验条件,探讨ATP合酶对呼吸通量控制的贡献与钙诱导的大鼠、家兔和豚鼠心脏线粒体琥珀酸氧化的激活之间的相关性。心脏线粒体呼吸对温度从37℃降至28℃的敏感性依次为家兔>豚鼠>大鼠。Ca2+对状态3呼吸下琥珀酸氧化速率的影响是物种和温度依赖的,范围从0(大鼠,37℃)到+44%(兔,28℃)。对于所有实验动物的线粒体,生理浓度范围内Ca2+的增加没有改变状态2呼吸速率。Ca2+对状态3呼吸的刺激作用在28℃时比在37℃时更为明显,呼吸子系统仅在兔心脏线粒体中对Ca2+离子敏感。Ca2+在状态3中刺激琥珀酸盐氧化的能力与ATP合酶对呼吸通量的控制之间存在高度正相关,这为证实Ca2+离子刺激ATP合酶提供了论据。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Contribution of ATP synthase to stimulation of respiration by Ca2+ in heart mitochondria.

A variety of experimental conditions were applied with the aim to estimate the correlation between the contribution of ATP synthase to the respiratory flux control and the calcium-induced activation of succinate oxidation in heart mitochondria isolated from rat, rabbit and guinea pig. The sensitivity of respiration in heart mitochondria to the decrease in temperature from 37 degrees C to 28 degrees C decreases in the order rabbit > guinea pig > rat. Ca2+ effect on succinate oxidation rate in state 3 respiration was species- and temperature-dependent and ranged from 0 (rat, 37 degrees C) to +44% (rabbit, 28 degrees C). For mitochondria from all experimental animals, the increase of Ca2+ in physiological range of concentration did not change state 2 respiration rate, and the stimulatory effect of Ca2+ on state 3 respiration was more pronounced at 28 degrees C than at 37 degrees C. The respiratory subsystem was sensitive to Ca2+ ions only in rabbit heart mitochondria. A high positive correlation between Ca2+ ability to stimulate succinate oxidation in state 3 and the control exerted by ATP synthase over the respiratory flux provides argument confirming stimulation of ATP synthase by Ca2+ ions.

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