首页> 外文期刊>The Journal of Experimental Biology >Effects of temperature and cadmium exposure on the mitochondria of oysters (Crassostrea virginica) exposed to hypoxia and subsequent reoxygenation
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Effects of temperature and cadmium exposure on the mitochondria of oysters (Crassostrea virginica) exposed to hypoxia and subsequent reoxygenation

机译:温度和镉暴露对暴露于低氧和随后复氧的牡蛎线粒体的影响

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摘要

Intertidal bivalves are commonly exposed to multiple stressors including periodic hypoxia, temperature fluctuations and pollution, which can strongly affect energy metabolism. We used top-down control and elasticity analyses to determine the interactive effects of intermittent hypoxia, cadmium (Cd) exposure and acute temperature stress on mitochondria of the eastern oyster Crassostrea virginica. Oysters were acclimated at 20 degrees C for 30 days in the absence or presence of 50 mu g l(-1) Cd and then subjected to a long-term hypoxia (6 days at <0.5% O-2 in seawater) followed by normoxic recovery. Mitochondrial function was assessed at the acclimation temperature (20 degrees C), or at elevated temperature (30 degrees C) mimicking acute temperature stress in the intertidal zone. In the absence of Cd or temperature stress, mitochondria of oysters showed high resilience to transient hypoxia. In control oysters at 20 degrees C, hypoxia/reoxygenation induced elevated flux capacity of all three studied mitochondrial subsystems (substrate oxidation, phosphorylation and proton leak) and resulted in a mild depolarization of resting mitochondria. Elevated proton conductance and enhanced capacity of phosphorylation and substrate oxidation subsystems may confer resistance to hypoxia/reoxygenation stress in oyster mitochondria by alleviating production of reactive oxygen species and maintaining high aerobic capacity and ATP synthesis rates during recovery. Exposure to environmental stressors such as Cd and elevated temperatures abolished the putative adaptive responses of the substrate oxidation and phosphorylation subsystems, and strongly enhanced proton leak in mitochondria of oysters subjected to hypoxia/reoxygenation stress. Our findings suggest that Cd exposure and acute temperature stress may lead to the loss of mitochondrial resistance to hypoxia and reoxygenation and thus potentially affect the ability of oysters to survive periodic oxygen deprivation in coastal and estuarine habitats.
机译:潮间双壳类动物通常暴露于多种应激源,包括周期性的缺氧,温度波动和污染,这会严重影响能量代谢。我们使用自上而下的控制和弹性分析来确定间歇性缺氧,镉(Cd)暴露和急性温度胁迫对东部牡蛎Crassostrea virginica线粒体的相互作用。牡蛎在不存在或存在50μggl(-1)Cd的情况下在20°C适应30天,然后经受长期缺氧(海水中O-2 <0.5%时为6天),然后恢复常氧。在适应温度(20摄氏度)或模仿潮间带急性温度胁迫的高温(30摄氏度)下评估线粒体功能。在没有Cd或温度胁迫的情况下,牡蛎的线粒体显示出对短暂缺氧的高复原力。在20摄氏度的对照牡蛎中,低氧/复氧诱导所有三个研究的线粒体子系统(底物氧化,磷酸化和质子泄漏)通量增加,并导致线粒体的轻度去极化。质子传导性的提高以及磷酸化和底物氧化子系统能力的增强,可通过减轻活性氧的产生并在恢复过程中保持高需氧能力和ATP合成速率,从而赋予牡蛎线粒体耐缺氧/复氧的能力。暴露于镉和高温等环境胁迫下,消除了底物氧化和磷酸化子系统的假定适应性反应,并大大增强了经受缺氧/复氧应激作用的牡蛎线粒体的质子泄漏。我们的发现表明,镉暴露和急性温度胁迫可能会导致线粒体对缺氧和复氧的抵抗力丧失,从而潜在影响牡蛎在沿海和河口生境中定期缺氧生存的能力。

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