Dourado Priscila Leocádia Rosa, da Silva Danilo Grunig Humberto, Alves Thiago Caique, de Almeida Eduardo Alves
UNESP - Universidade Estadual Paulista, Departamento de Química e Ciências Ambientais, São Paulo, Brazil.
Universidade Federal de Mato Grosso do Sul, Câmpus de Três Lagoas, Três Lagoas, Mato Grosso do Sul, Brazil.
Aquat Toxicol. 2025 Jan;278:107163. doi: 10.1016/j.aquatox.2024.107163. Epub 2024 Nov 12.
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) and how these responses are affected by simultaneous exposure to the insecticide fipronil (0.1 and 0.5 µg L). 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.
已知急性缺氧会增加活性氧（ROS）的生成，从而导致抗氧化防御机制的调节。污染物暴露会在缺氧事件期间增强ROS的生成，并损害抗氧化防御机制，增加耐缺氧鱼类（如尼罗罗非鱼，Oreochromis niloticus）对氧化应激的易感性。本研究的目的是评估尼罗罗非鱼对急性（3小时和8小时）中度缺氧（溶解氧≤2毫克/升）的氧化应激反应，以及同时暴露于杀虫剂氟虫腈（0.1和0.5微克/升）如何影响这些反应。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，同时也增加了肝脏中的过氧化氢酶（CAT）和谷胱甘肽S-转移酶（GST）活性。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，缺氧降低了红细胞中的DNA损伤（彗星试验）。氟虫腈暴露3小时在常氧和缺氧条件下均降低了鳃中的CAT活性。8小时后，氟虫腈和缺氧的联合作用增加了鳃中的GR活性。在肝脏中，缺氧条件下氟虫腈暴露3小时增加了CAT和GR活性；8小时后，CAT降低，GST增加。常氧条件下氟虫腈暴露8小时也增加了GR活性。所有处理均降低了鳃中的脂质过氧化水平，但在肝脏中，常氧条件下氟虫腈暴露3小时后脂质过氧化增加。此外，缺氧条件下氟虫腈暴露3小时和8小时增加了红细胞中的DNA损伤，而常氧条件下氟虫腈暴露8小时则降低了DNA损伤，这表明DNA修复机制被激活。结果表明，氟虫腈和缺氧暴露均显著调节尼罗罗非鱼的氧化应激参数，并且这些因素的联合作用产生了更明显的影响。
