Acute hypoxia is known to increase the generation of reactive oxygen species (ROS), leading to modulation in antioxidant defenses. Pollutant exposure can potentiate ROS generation during hypoxic events and impair antioxidant defenses, increasing the susceptibility of hypoxia-tolerant fishes, such as the Nile tilapia (Oreochromis niloticus), to oxidative stress. The purpose of this study was to evaluate oxidative stress responses of O. niloticus to acute (3 and 8 h) moderate hypoxia (dissolved oxygen ≤2 mg/L−1) and how these responses are affected by simultaneous exposure to the insecticide fipronil (0.1 and 0.5 µg L−1). Hypoxia exposure for 3 h caused an increase in glutathione peroxidase (GPx) activity in the gill and also increased catalase (CAT) and glutathione S-transferase (GST) activities in the liver. After 8 h of hypoxia, glutathione reductase (GR) activity increased. DNA damage (comet assay) in erythrocytes was reduced by hypoxia after 3 and 8 h. Fipronil exposure for 3 h decreased CAT activity in the gill, both under normoxia and hypoxia. After 8 h, the combination of fipronil and hypoxia increased GR activity in the gill. In the liver, fipronil exposure under hypoxia for 3 h increased CAT and GR activities; after 8 h, CAT was decreased, and GST increased. GR was also increased by fipronil under normoxia for 8 h. All treatments reduced lipid peroxidation levels in the gills, but in the liver, lipid peroxidation was increased by fipronil after 3 h under normoxia. Moreover, fipronil exposure under hypoxia for 3 and 8 h increased DNA damage in erythrocytes, while 8 h of fipronil exposure under normoxia decreased it, suggesting the activation of DNA repair mechanisms. Results show that both fipronil and hypoxia exposure significantly modulate the oxidative stress parameters of O. niloticus and that the combination of these factors produces more pronounced effects.

中文翻译：

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氟虫腈暴露会改变尼罗罗非鱼 （Oreochromis niloticus） 对急性中度缺氧的氧化应激反应


已知急性缺氧会增加活性氧 （ROS） 的产生，导致抗氧化防御的调节。污染物暴露会增强低氧事件期间 ROS 的产生并损害抗氧化防御，从而增加耐缺氧鱼类（如尼罗罗非鱼 （Oreochromis niloticus））对氧化应激的敏感性。本研究的目的是评估 O. niloticus 对急性 （3 小时和 8 小时） 中度缺氧 （溶解氧 ≤2 mg/L-1） 的氧化应激反应，以及这些反应如何受到同时暴露于杀虫剂氟虫腈 （0.1 和 0.5 μg L-1） 的影响。缺氧暴露 3 小时导致鳃中谷胱甘肽过氧化物酶 （GPx） 活性增加，肝脏中过氧化氢酶 （CAT） 和谷胱甘肽 S-转移酶 （GST） 活性增加。缺氧 8 小时后，谷胱甘肽还原酶 （GR） 活性增加。3 小时和 8 小时后，缺氧减少了红细胞中的 DNA 损伤 （彗星测定）。氟虫腈暴露 3 小时降低了常氧和缺氧下鳃中的 CAT 活性。8 小时后，氟虫腈和缺氧的组合增加了鳃中的 GR 活性。在肝脏中，缺氧 3 h 氟虫腈暴露增加了 CAT 和 GR 活性;8 小时后，CAT 降低，GST 增加。在常氧下 8 小时，氟虫腈也增加了 GR。所有处理都降低了鳃中的脂质过氧化水平，但在肝脏中，在常氧下 3 小时后氟虫腈增加了脂质过氧化。此外，在缺氧下暴露氟虫腈 3 小时和 8 小时会增加红细胞中的 DNA 损伤，而在常氧条件下暴露氟虫腈 8 小时会减少损伤，表明 DNA 修复机制的激活。 结果表明，氟虫腈和缺氧暴露均显著调节 O. niloticus 的氧化应激参数，并且这些因素的组合产生了更显着的影响。