Inhibition of pro-oxidant-induced mitochondrial pyridine nucleotide hydrolysis and calcium release by 4-hydroxynonenal.
Inhibition of pro-oxidant-induced mitochondrial pyridine nucleotide hydrolysis and calcium release by 4-hydroxynonenal.
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DOI：
10.1042/bj2690735
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发表时间：
1990-08
期刊：
影响因子：
--
通讯作者：
C. Richter;P. Meier
中科院分区：
文献类型：
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作者：
C. Richter;P. Meier
线粒体内和线粒体外Ca 2+参与重要的细胞过程。本文研究了4-羟基壬烯醛（HNE）对促氧化剂诱导的大鼠肝线粒体Ca ~（2+）释放的影响。Ca 2+运动的线粒体内膜，吡啶核苷酸氧化还原状态和吡啶（烟酰胺）核苷酸水解进行了分析。HNE不影响线粒体对Ca ~（2+）的摄取，但以浓度依赖方式抑制叔丁基过氧化氢（tbh）诱导的Ca ~（2+）释放。用约50 μ M-HNE实现总抑制。HNE也能抑制促氧化剂四氧嘧啶诱导的Ca ~（2+）释放。氧化的吡啶核苷酸，诱导TBH通过谷胱甘肽过氧化物酶，谷胱甘肽还原酶和能量连接的转氢酶的协同作用，不受影响，高达50微M-HNE。相反，HNE以浓度依赖性方式抑制吡啶核苷酸水解。这些数据表明，HNE毒性可能部分归因于受损的线粒体内Ca 2+稳态。
Intra- and extra-mitochondrial Ca2+ participates in vital cellular processes. This work investigates the influence of 4-hydroxynonenal (HNE) on pro-oxidant-induced Ca2+ release from rat liver mitochondria. Ca2+ movements across the mitochondrial inner membrane, the pyridine nucleotide redox state and pyridine (nicotinamide) nucleotide hydrolysis were analysed. HNE did not influence Ca2+ uptake by mitochondria, but inhibited in a concentration-dependent manner Ca2+ release induced by t-butylhydroperoxide (tbh). Total inhibition was achieved with about 50 microM-HNE. Ca2+ release induced by the pro-oxidant alloxan was also inhibited by HNE. Oxidation of pyridine nucleotides, induced by tbh through the concerted action of glutathione peroxidase, glutathione reductase and the energy-linked transhydrogenase, was not affected by up to 50 microM-HNE. In contrast, HNE inhibited pyridine nucleotide hydrolysis in a concentration-dependent manner. The data suggest that HNE toxicity may be in part attributed to an impaired intramitochondrial Ca2+ homeostasis.