Department of Biology, McMaster University, Hamilton, ON, Canada, L8S 4L8
Department of Biology, McMaster University, Hamilton, ON, Canada, L8S 4L8.
J Exp Biol. 2020 Jul 6;223(Pt 13):jeb222877. doi: 10.1242/jeb.222877.
Hypoxia is common in aquatic environments, and exposure to hypoxia followed by re-oxygenation is often believed to induce oxidative stress. However, there have been relatively few studies of reactive oxygen species (ROS) homeostasis and oxidative status in fish that experience natural hypoxia-re-oxygenation cycles. We examined how exposure to acute hypoxia (2 kPa O) and subsequent re-oxygenation (to 20 kPa O) affects redox status, oxidative damage and anti-oxidant defenses in estuarine killifish (), and whether these effects were ameliorated or potentiated by prolonged (28 days) acclimation to either constant hypoxia or intermittent cycles of nocturnal hypoxia (12 h:12 h normoxia:hypoxia). Acute hypoxia and re-oxygenation led to some modest and transient changes in redox status, increases in oxidized glutathione, depletion of scavenging capacity and oxidative damage to lipids in skeletal muscle. The liver had greater scavenging capacity, total glutathione concentrations and activities of anti-oxidant enzymes (catalase, glutathione peroxidase) than muscle, and generally experienced less variation in glutathiones and lipid peroxidation. Unexpectedly, acclimation to constant hypoxia or intermittent hypoxia led to a more oxidizing redox status (muscle and liver) and it increased oxidized glutathione (muscle). However, hypoxia-acclimated fish exhibited little to no oxidative damage (as reflected by lipid peroxidation and aconitase activity), in association with improvements in scavenging capacity and catalase activity in muscle. We conclude that hypoxia acclimation leads to adjustments in ROS homeostasis and oxidative status that do not reflect oxidative stress, but may instead be part of the suite of responses that killifish use to cope with chronic hypoxia.
缺氧在水生环境中很常见，通常认为暴露于缺氧后再复氧会诱导氧化应激。然而，经历自然缺氧-复氧循环的鱼类中，关于活性氧（ROS）稳态和氧化状态的研究相对较少。我们研究了急性缺氧（2 kPa O）和随后复氧（至 20 kPa O）如何影响河口丽鱼（）的氧化还原状态、氧化损伤和抗氧化防御，以及这些影响是否通过长期（28 天）适应恒低氧或间歇性夜间缺氧（12 h：12 h 常氧：缺氧）而得到改善或增强。急性缺氧和复氧导致氧化还原状态的一些适度和短暂变化，氧化型谷胱甘肽增加，清除能力耗竭，骨骼肌脂质氧化损伤。肝脏的清除能力、总谷胱甘肽浓度和抗氧化酶（过氧化氢酶、谷胱甘肽过氧化物酶）活性高于肌肉，通常谷胱甘肽和脂质过氧化变化较小。出乎意料的是，恒低氧或间歇性低氧适应导致更氧化的氧化还原状态（肌肉和肝脏），并增加了氧化型谷胱甘肽（肌肉）。然而，缺氧适应的鱼类几乎没有或没有氧化损伤（如脂质过氧化和乌头酸酶活性所反映的那样），同时肌肉的清除能力和过氧化氢酶活性提高。我们得出结论，缺氧适应导致 ROS 稳态和氧化状态的调整，这些调整不反映氧化应激，而可能是丽鱼用于应对慢性缺氧的一系列反应的一部分。
