Crucial role of membrane potential in heat stress-induced overproduction of reactive oxygen species in avian skeletal muscle mitochondria.

Crucial role of membrane potential in heat stress-induced overproduction of reactive oxygen species in avian skeletal muscle mitochondria.
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DOI:
10.1371/journal.pone.0064412
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发表时间:
2013
期刊:
影响因子:
3.7
通讯作者:
Toyomizu M
Toyomizu M
中科院分区:
综合性期刊3区
文献类型:
--
作者:
Kikusato M;Toyomizu M

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热应激是导致氧化应激的环境因素。我们先前发现,急性热应激刺激鸟类骨骼肌线粒体产生活性氧物种(ROS),并伴随着线粒体膜电位(ΔΨ)的增加,这是由于电子传递链增加底物氧化所致。我们还发现,热暴露降低了禽解偶联蛋白(AvUCP)的表达。本研究阐明了ΔΨ是否是急性热应激引起的ROS过量产生的主要决定因素,以及ΔΨ表达的降低是否是导致AvUCP表达升高的原因。对照(24℃)和急性热应激(34℃,12h)的鸟类表现出琥珀酸驱动的线粒体ROS生成增加,ΔΨ的升高表明,这种增加在热应激组显著高于对照组。在谷氨酸/苹果酸供能的线粒体中,尽管热应激组线粒体ΔΨ显著高于对照组,但两组间ROS的产生无明显差异。此外,与对照组相比,用琥珀酸/谷氨酸或琥珀酸/苹果酸供电的线粒体在热应激组表现出更多的ROS产生和ΔΨ。这些结果表明,琥珀酸氧化在热应激诱导的骨骼肌线粒体ROS过量产生中起重要作用。与热应激导致avUCP表达下降的观点一致,热暴露组的质子泄漏减少,这可能是由UCP(GDP抑制和花生四烯酸敏感的部分)介导的。我们认为,急性热应激诱导的线粒体ROS的过量产生可能依赖于ΔΨ,这可能不仅是底物氧化增加的结果,也可能是线粒体avUCP含量下降的结果。
Heat stress is an environmental factor that causes oxidative stress. We found previously that acute heat stress stimulates the production of reactive oxygen species (ROS) in the skeletal muscle mitochondria of birds, and that this was accompanied by an increase of the mitochondrial membrane potential (ΔΨ) due to increased substrate oxidation by the electron transport chain. We also showed that avian uncoupling protein (avUCP) expression is decreased by the heat exposure. The present study clarifies whether ΔΨ is a major determinant of the overproduction of ROS due to acute heat stress, and if the decrease in avUCP expression is responsible for the elevation in ΔΨ. Control (24°C) and acute heat-stressed (34°C for 12 h) birds exhibited increased succinate-driven mitochondrial ROS production as indicated by an elevation of ΔΨ, with this increase being significantly higher in the heat-stressed group compared with the control group. In glutamate/malate-energized mitochondria, no difference in the ROS production between the groups was observed, though the mitochondrial ΔΨ was significantly higher in the heat-stressed groups compared with the control group. Furthermore, mitochondria energized with either succinate/glutamate or succinate/malate showed increased ROS production and ΔΨ in the heat-stressed group compared with mitochondria from the control group. These results suggest that succinate oxidation could play an important role in the heat stress-induced overproduction of mitochondrial ROS in skeletal muscle. In agreement with the notion of a decrease in avUCP expression in response to heat stress, proton leak, which was likely mediated by UCP (that part which is GDP-inhibited and arachidonic acid-sensitive), was reduced in the heat-exposed group. We suggest that the acute heat stress-induced overproduction of mitochondrial ROS may depend on ΔΨ, which may in turn result not only from increased substrate oxidation but also from a decrease in the mitochondrial avUCP content.
DOI: 10.1042/bj20081386
发表时间: 2009-01-01
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