期刊
MECHANISMS OF AGEING AND DEVELOPMENT
卷 122, 期 10, 页码 1073-1086出版社
ELSEVIER IRELAND LTD
DOI: 10.1016/S0047-6374(01)00242-1
关键词
aging; calcium; cardioprotection; diazoxide; K-ATP channel; senescence
资金
- NHLBI NIH HHS [HL-07111, HL-64822] Funding Source: Medline
In senescence, endogenous mechanisms of cardioprotection are apparently attenuated resulting in increased vulnerability to ischemia-reperfusion. In particular, mitochondria, which are essential in maintaining cardiac energetic and ionic homeostasis, are susceptible to Ca2+ overload, a component of metabolic injury. However, effective means of protecting senescent mitochondria are lacking. Here, mitochondrial function and structure were assessed using ion-selective mini-electrodes, high-performance liquid chromatography and electron microscopy. Aging decreased ADP-induced oxygen consumption and prolonged the time associated with ADP to ATP conversion, which manifested as a reduced rate of oxidative phosphorylation. Aging also reduced mitochondrial Ca2+ handling, and increased Ca2+-induced mitochondrial damage. Diazoxide, a potassium channel opener, reduced Ca2+ loading and protected the functional and structural integrity of senescent mitochondria from Ca2+-induced injury. In this way, the present study identifies the potential usefulness for pharmacotherapy in protecting vulnerable senescent mitochondria from conditions of Ca2+ overload, such as: ischemia-reperfusion. (C) 2001 Elsevier Science Ireland Ltd. All rights reserved.
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