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首页> 外文期刊>American Journal of Physiology >Cadmium affects metabolic responses to prolonged anoxia and reoxygenation in eastern oysters (Crassostrea virginica).
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Cadmium affects metabolic responses to prolonged anoxia and reoxygenation in eastern oysters (Crassostrea virginica).

机译：镉影响东部牡蛎（Crassostrea virginica）对长时间缺氧和复氧的代谢反应。

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摘要

Benthic marine organisms such as mollusks are often exposed to periodic oxygen deficiency (due to the tidal exposure and/or seasonal expansion of the oxygen-deficient dead zones) and pollution by metals [e.g., cadmium, (Cd)]. These stressors can strongly affect mollusks' survival; however, physiological mechanisms of their combined effects are not fully understood. We studied the effects of Cd exposure on metabolic responses to prolonged anoxia and subsequent recovery in anoxia-tolerant intertidal mollusks Crassostrea virginica (eastern oysters). Anoxia led to an onset of anaerobiosis indicated by accumulation of l-alanine, acetate, and succinate. Prolonged anoxia (for 6 days) caused a decline in the maximum activity of electron transport chain and ADP-stimulated (state 3) oxygen uptake by mitochondria (MO(2)), but no change in the resting (state 4) MO(2) of oyster mitochondria, along with a slight but significant reduction of mitochondrial respiratory control ratio. During reoxygenation, there was a significant overshoot of mitochondrial MO(2) (by up to 70% above the normoxic steady-state values) in control oysters. Mild mitochondrial uncoupling during prolonged shutdown in anoxic tissues and a subsequent strong stimulation of mitochondrial flux during recovery may help to rapidly restore redox status and protect against elevated reactive oxygen species formation in oysters. Exposure to Cd inhibits anaerobic metabolism, abolishes reoxygenation-induced stimulation of mitochondrial MO(2), and leads to oxidative stress (indicated by accumulation of DNA lesions) and a loss of mitochondrial capacity during postanoxic recovery. This may result in increased sensitivity to intermittent hypoxia and anoxia in Cd-exposed mollusks and will have implications for their survival in polluted estuaries and coastal zones.
机译：底栖海洋生物（如软体动物）通常会暴露于周期性缺氧（由于潮汐暴露和/或缺氧死区的季节性扩展）和金属[例如镉（Cd）]污染。这些应激源可以极大地影响软体动物的生存。然而，它们的综合作用的生理机制尚不完全清楚。我们研究了镉暴露对长时间缺氧的潮汐软体动物代谢反应的影响，以及随后在耐潮性软体动物Crassostrea virginica（东部牡蛎）中恢复的过程。缺氧导致1-丙氨酸，乙酸盐和琥珀酸盐的积累表明厌氧菌的发作。长时间缺氧（持续6天）导致线粒体（MO（2））吸收电子传输链和ADP刺激（状态3）的最大摄氧量下降（MO（2）），但静止状态（状态4）MO（2）不变）牡蛎线粒体，以及线粒体呼吸控制率的轻微但显着降低。在复氧过程中，控制牡蛎的线粒体MO（2）明显过冲（比常氧稳态值高70％）。缺氧组织长时间关闭期间轻度的线粒体解偶联以及随后在恢复过程中对线粒体通量的强烈刺激可能有助于迅速恢复氧化还原状态并防止牡蛎中活性氧物种的形成增加。暴露于Cd会抑制无氧代谢，废除复氧诱导的线粒体MO（2）刺激，并导致氧化应激（由DNA损伤的积累指示）和缺氧后恢复过程中线粒体能力的丧失。这可能导致暴露于Cd的软体动物对间歇性缺氧和缺氧的敏感性增加，并将对其在污染河口和沿海地区的生存产生影响。

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