Department of Applied Environmental Science (ITM), Stockholm University, Stockholm, Sweden.
Aquat Toxicol. 2013 Feb;127:46-53. doi: 10.1016/j.aquatox.2012.01.022. Epub 2012 Feb 6.
Fitness and survival of an organism depend on its ability to mount a successful stress response when challenged by exposure to damaging agents. We hypothesized that co-exposure to contaminants may exacerbate oxidative stress in hypoxia-challenged benthic animals compromising their ability to recover upon reoxygenation. This was tested using the amphipod Monoporeia affinis exposed to hypoxia followed by reoxygenation in sediments collected in polluted and pristine areas. In both sediment types, oxygen radical absorbance capacity (ORAC) and antioxidant enzyme activities [superoxide dismutase (SOD) and catalase (CAT)] increased during hypoxia, suggesting that M. affinis has a strategy of preparation for oxidative stress that facilitates recovery after a hypoxic episode. Exposure to contaminants altered this anticipatory response as indicated by higher baselines of ORAC and SOD during hypoxia and no response upon reoxygenation. This coincided with significantly elevated oxidative damage evidenced by a marked reduction in glutathione redox status (ratio of reduced GSH/oxidized GSSG) and an increase in lipid peroxidation (TBARS levels). Moreover, RNA:DNA ratio, a proxy for protein synthetic activity, decreased in concert with increased TBARS, indicating a linkage between oxidative damage and fitness. Finally, inhibited acetylcholinesterase (AChE) activity in animals exposed to contaminated sediments suggested a neurotoxic impact, whereas significant correlations between AChE and oxidative biomarkers may indicate connections with redox state regulation. The oxidative responses in pristine sediments suggested a typical scenario of ROS production and removal, with no apparent oxidative damage. By contrast, co-exposure to contaminants caused greater increase in antioxidants, lipid peroxidation, and slowed recovery from hypoxia as indicated by CAT, GSH/GSSG, TBARS and AChE responses. These results support the hypothesized potential of xenobiotics to hamper ability of animals to cope with fluctuating hypoxia. They also emphasize the importance of understanding interactions between antioxidant responses to different stressors and physiological mechanisms of oxidative damage.
生物体的健康和生存取决于其在受到损伤性物质暴露时，能否成功地应对压力并做出反应。我们假设，污染物的共暴露可能会加剧缺氧条件下底栖动物的氧化应激，从而影响它们在复氧后的恢复能力。我们使用双齿围沙蚕（Monoporeia affinis）进行了测试，这种桡足类动物在受到缺氧胁迫后，又在污染和未受污染地区采集的沉积物中经历了复氧过程。在这两种沉积物类型中，氧自由基吸收能力（ORAC）和抗氧化酶活性（超氧化物歧化酶（SOD）和过氧化氢酶（CAT））在缺氧期间均有所增加，这表明双齿围沙蚕具有应对氧化应激的策略，有助于其在缺氧事件后恢复。污染物的暴露改变了这种预期反应，表现为缺氧期间 ORAC 和 SOD 的基线更高，而复氧时则没有反应。这与氧化损伤明显增加的情况相吻合，表现为谷胱甘肽还原状态（还原型 GSH/氧化型 GSSG 比值）显著降低和脂质过氧化（TBARS 水平）增加。此外，RNA:DNA 比值（蛋白质合成活性的替代指标）随着 TBARS 的增加而降低，表明氧化损伤与健康状况之间存在联系。最后，暴露于污染沉积物中的动物乙酰胆碱酯酶（AChE）活性受到抑制，表明存在神经毒性影响，而 AChE 与氧化生物标志物之间的显著相关性可能表明其与氧化还原状态调节有关。未受污染沉积物中的氧化反应表明存在典型的活性氧（ROS）产生和清除情况，没有明显的氧化损伤。相比之下，污染物的共暴露导致抗氧化剂、脂质过氧化和 CAT、GSH/GSSG、TBARS 和 AChE 反应指示的缺氧恢复速度变慢等方面的氧化应激反应增加。这些结果支持了污染物可能会干扰动物应对波动缺氧能力的假设。它们还强调了理解不同应激源的抗氧化反应与氧化损伤生理机制之间相互作用的重要性。
