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本文应用分离的鼠肝线粒体,研究了血卟啉光敏化反应在不同光照时间和血卟啉浓度条件下对线粒体功能的影响.通过对线粒体生物能力学参数诸如3态和4态呼吸速率、呼吸控制率、跨膜电位、以及H~+-ATP酶水解和合成活性、呼吸链复合体Ⅱ+Ⅲ质子转位和内膜质子回漏的测定,首次直接证明:线粒体内膜质子漏和由此引起的跨膜质子梯度的破坏是血卟啉光敏化反应导致线粒体氧化磷酸化功能扒伤的机制.
In this paper, isolated rat liver mitochondria were used to study the effect of hematoporphyrin photosensitizing reaction on mitochondrial function under different illumination time and hematoporphyrin concentration conditions. Through the mitochondrial bioavailability parameters such as 3-state and 4-state respiration rates, respiration The control rate, transmembrane potential, and the hydrolysis and synthesis activity of H~+-ATPase, the proton translocation of the respiratory chain complex II+III, and the leakage of intimal protons directly demonstrate for the first time that the mitochondrial inner membrane proton leaks and thus Destruction of the transmembrane proton gradient is the mechanism of the oxidative phosphorylation of mitochondria by the photosensitizing reaction of hematoporphyrin.