Serviddio G, Bellanti F, Romano A D, Tamborra R, Rollo T, Altomare E, Vendemiale G
Institute of Internal Medicine, Department of Medical and Occupational Sciences, University of Foggia, Foggia, Italy.
Redox Rep. 2007;12(1):91-5. doi: 10.1179/135100007X162112.
Aging is associated with a decline in performance in many organs and loss of physiological performance can be due to free radicals. Mitochondria are incompletely coupled: during oxidative phosphorylation some of the redox energy is dissipated as natural proton leak across the inner membrane. To verify whether proton leak occurs in mitochondria during aging, we measured the mitochondrial respiratory chain activity, membrane potential and proton leak in liver, kidneys and heart of young and old rats. Mitochondria from old rats showed normal rates of Complex I and Complex II respiration. However, they had a lower membrane potential compared to mitochondria from younger rats. In addition, they exhibited an increased rate of proton conductance which partially dissipated the mitochondrial membrane potential when the rate of electron transport was suppressed. This could compromise energy homeostasis in aging cells in conditions that require additional energy supply and could minimize oxidative damage to DNA.
衰老与许多器官的功能衰退相关,生理功能的丧失可能归因于自由基。线粒体的偶联不完全:在氧化磷酸化过程中,一些氧化还原能量以质子自然跨内膜泄漏的形式耗散。为了验证衰老过程中线粒体是否发生质子泄漏,我们测量了年轻和老年大鼠肝脏、肾脏和心脏中的线粒体呼吸链活性、膜电位和质子泄漏。老年大鼠的线粒体显示出正常的复合体I和复合体II呼吸速率。然而,与年轻大鼠的线粒体相比,它们的膜电位较低。此外,当电子传递速率受到抑制时,它们表现出质子传导速率增加,这部分耗散了线粒体膜电位。在需要额外能量供应的情况下,这可能会损害衰老细胞中的能量稳态,并可能将对DNA的氧化损伤降至最低。