Please use this identifier to cite or link to this item: http://hdl.handle.net/10397/14908
Title: Endomorphins and morphine limit anoxia-reoxygenation-induced brain mitochondrial dysfunction in the mouse
Authors: Feng, Y
Lu, Y
Lin, X
Gao, Y
Zhao, Q
Li, W
Wang, R
Keywords: Anoxia-reoxygenation
Brain mitochondria
Endomorphins
Morphine
Issue Date: 2008
Publisher: Pergamon-Elsevier Science Ltd
Source: Life sciences, 2008, v. 82, no. 13-14, p. 752-763 How to cite?
Journal: Life Sciences 
Abstract: The protection of brain mitochondria from oxidative stress is an important therapeutic strategy against ischemia-reperfusion injury and neurodegenerative disorders. Isolated brain mitochondria subjected to a 5 min period of anoxia followed by 5 min reoxygenation mirrored the effect of oxidative stress in the brain. The present study attempts to evaluate the protective effects of endomorphin 1 (EM1), endomorphin 2 (EM2), and morphine (Mor) in an in vitro mouse brain mitochondria anoxia-reoxygenation model. Endomorphins (EM1/2) and Mor were added to mitochondria prior to anoxia or reoxygenation. EM1/2 and Mor markedly improved mitochondrial respiratory activity with a decrease in state 4 and increases in state 3, respiratory control ratio (RCR) and the oxidative phosphorylation efficiency (ADP/O ratio), suggesting that they may play a protective role in mitochondria. These drugs inhibited alterations in mitochondrial membrane fluidity, lipoperoxidation, and cardiolipin (CL) release, which indicates protection of the mitochondrial membranes from oxidative damage. The protective effects of these drugs were concentration-dependent. Furthermore, these drugs blocked the enhanced release of cytochrome c (Cyt c), and consequently inhibited the cell apoptosis induced by the release of Cyt c. Our results suggest that EM1/2 and Mor effectively protect brain mitochondria against oxidative stresses induced by in vitro anoxia-reoxygenation and may play an important role in the prevention of deleterious effects during brain ischemia-reperfusion and neurodegenerative diseases.
URI: http://hdl.handle.net/10397/14908
DOI: 10.1016/j.lfs.2008.01.004
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