Analyzing the uncorrected error of dilution water demand for the dilution biochemical oxygen demand method

中國醫藥大學機構典藏 China Medical University Repository, Taiwan > 公共衛生學院 > 環境醫學研究所(已停用) > 期刊論文 > Item 310903500/28882

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题名:	Analyzing the uncorrected error of dilution water demand for the dilution biochemical oxygen demand method
作者:	Chiang, CF;Wu, YS;Young, JC
贡献者:	公共衛生學院環醫所;China Med Univ, Inst Environm Hlth, Taichung, Taiwan;Natl Chung Hsing Univ, Dept Environm Engn, Taichung 40227, Taiwan;Univ Arkansas, Dept Civil Engn, Fayetteville, AR 72701 USA
日期:	2004
上传时间:	2010-09-24 13:59:13 (UTC+8)
出版者:	WATER ENVIRONMENT FEDERATION
摘要:	Oxidative stress-induced mitochondrial dysfunction has been shown to play a crucial role in the pathogenesis of a wide range of diseases. Protecting mitochondrial function, therefore, is vital for cells to survive during these disease processes. In this study, we demonstrate that melatonin, a chief secretory product of the pineal gland, readily rescued mitochondria from oxidative stress-induced dysfunction and effectively prevented subsequent apoptotic events and death in rat brain astrocytes (RBA-1). The early protection provided by melatonin in mitochondria of intact living cells was investigated by the application of time-lapse conventional, confocal, and multiphoton fluorescent imaging microscopy coupled with noninvasive mitochondria-targeted fluorescent probes. In particular, we observed that melatonin effectively prevented exogenously applied H2O2-induced mitochondrial swelling in rat brain astrocytes at an early time point (within 10 min) and subsequently reduced apoptotic cell death (150 min later). Other early apoptotic events such as plasma membrane exposure of phosphatidyl serine and the positive YOPRO-1 staining of the early apoptotic nucleus were also prevented by melatonin. A mechanistic study at the mitochondrial level related to the early protection provided by melatonin revealed that the indole molecule significantly reduced mitochondrial reactive oxygen species (ROS) formation induced by H2O2 stress. Melatonin also prevented mitochondrial ROS generation caused by other organic hydroperoxides including tert-butyl hydroperoxide and cumene hydroperoxide. This antioxidative effect of melatonin is more potent than that of vitamin E. Via its ability to reduce mitochondrial ROS generation, melatonin prevented H2O2-induced mitochondrial calcium overload, mitochondrial membrane potential depolarization, and the opening of the mitochondrial permeability transition (MPT) pore. As a result, melatonin blocked MPT-dependent cytochrome c release, the downstream activation of caspase 3, the condensation and karyorrhexis of the nucleus and apoptotic fragmentation of nuclear DNA. Thus, the powerful mitochondrial protection provided by melatonin reinforces its therapeutic potential to combat a variety of oxidative stress-induced mitochondrial dysfunctions as well as mitochondria-mediated apoptosis in various diseases.
關聯:	WATER ENVIRONMENT RESEARCH 76(3):238-244
显示于类别:	[環境醫學研究所(已停用)] 期刊論文

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