Effect of heat stress-induced production of mitochondrial reactive oxygen species on NADPH oxidase and heme oxygenase-1 mRNA levels in avian muscle cells
Effect of heat stress-induced production of mitochondrial reactive oxygen species on NADPH oxidase and heme oxygenase-1 mRNA levels in avian muscle cells
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DOI：
10.1016/j.jtherbio.2015.04.005
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发表时间：
2015-08-01
影响因子：
2.7
通讯作者：
Toyomizu, Masaaki
中科院分区：
文献类型：
--
作者：
Kikusato, Motoi;Yoshida, Hayami;Toyomizu, Masaaki
热应激是引起细胞氧化障碍的主要因素。在本研究中，我们研究了培养的禽类肌肉细胞在热应激下活性氧（ROS）过量产生的机制，并重点研究了线粒体超氧阴离子与热应激细胞中NADPH氧化酶（NOX）、超氧化物歧化酶（SOD）和血红素氧化酶-1 (HO-1) mRNA水平变化的相互作用。与正常细胞（37℃）相比，细胞暴露于热应激条件（41℃，6 h）导致线粒体超氧化物和细胞内ROS水平增加，羰基蛋白含量增加。线粒体解偶联剂2,4-二硝基苯酚降低热应激细胞内ROS水平。热应激细胞中NOX4 mRNA水平升高，HO-1 mRNA水平降低，而SOD1和SOD2 mRNA水平保持相对稳定。在热应激细胞培养基中添加超氧化物清除剂4-羟基TEMPO，使线粒体超氧化物和细胞内ROS水平以及NOX4和HO-1 mRNA水平恢复到接近正常值。我们认为，线粒体超氧化物的产生可能在增加禽类肌肉细胞的氧化损伤中发挥重要作用，可能是通过在热应激的禽类肌肉细胞中上调NOX4和下调HO-1来实现的。(C) 2015 Elsevier Ltd.版权所有。
Heat stress is a major factor inducing oxidative disturbance in cells. In the present study, we investigated the mechanism of overproduction of reactive oxygen species (ROS) in cultured avian muscle cells in response to heat stress, and also focused attention on the interaction of mitochondrial superoxide anions with altered NADPH oxidase (NOX), superoxide dismutase (SOD) and heme oxygenase-1 (HO-1) mRNA levels in heat-stressed cells. Exposure of cells to heat stress conditions (41 degrees C, 6 h) resulted in increased mitochondrial superoxide and intracellular ROS levels, and increased carbonyl protein content as compared with that of normal cells (37 degrees C). The mitochondrial uncoupler 2,4-dinitrophenol lowered intracellular ROS levels in heat-stressed cells. Heat stress increased NOX4 mRNA and decreased HO-1 mRNA levels, while SOD1 and SOD2 mRNA levels remained relatively stable in heat-stressed cells. Addition of the superoxide scavenger 4-hydroxy TEMPO to the culture medium of heat-stressed cells restored mitochondrial superoxide and intracellular ROS levels as well as NOX4 and HO-1 mRNA levels to near-normal values. We suggest that mitochondrial superoxide production could play an influential role in augmenting oxidative damage to avian muscle cells, possibly via the up-regulation of NOX4 and down-regulation of HO-1 in heat-stressed avian muscle cells. (C) 2015 Elsevier Ltd. All rights reserved.