Johannsson Ora E, Giacomin Marina, Sadauskas-Henrique Helen, Campos Derek F, Braz-Mota Susana, Heinrichs-Caldas Waldir D, Baptista Ramon, Wood Chris M, Almeida-Val Vera Maria F, Val Adalberto L
Laboratory of Ecophysiology and Molecular Evolution, Brazilian National Institute for Research of the Amazon, INPA, Manaus, AM, Brazil; Zoology Department, University of British Columbia, Vancouver, B.C. V6T 1Z4, Canada.
Laboratory of Ecophysiology and Molecular Evolution, Brazilian National Institute for Research of the Amazon, INPA, Manaus, AM, Brazil; Zoology Department, University of British Columbia, Vancouver, B.C. V6T 1Z4, Canada.
Comp Biochem Physiol A Mol Integr Physiol. 2018 Oct;224:53-67. doi: 10.1016/j.cbpa.2018.05.019. Epub 2018 Jun 1.
We examined whether oxidative damage and antioxidant responses are more likely to occur during hypoxia or re-oxygenation in hypoxia-tolerant fish, and whether there is an influence of the rate of re-oxygenation. An hypoxia/re-oxygenation experiment using wild-caught Cyphocharax abramoides (Rio Negro, Brazil), was designed to answer these questions. Lipid peroxidation (MDA), a measure of oxidative damage, and antioxidant activities (superoxide dismutase (SOD), glutathione peroxidase (GPx), antioxidant capacity against peroxyl radicals (ACAP)), were measured in brain, gill and liver tissues after normoxia, 3-h hypoxia (2.7 kPa), and 3-h hypoxia followed by 1-h or 3-h re-oxygenation, implemented either immediately or slowly (3.0 kPa·h). Critical oxygen tension of routine oxygen consumption rate (Pcrit) (4.1 kPa) and the P at loss of equilibrium (LOE) (1.7 kPa) were determined to set the experimental hypoxia exposure. The Regulation Index, a measure of oxyregulation with declining P, was 0.32. Oxidative damage occurred during hypoxia: no additional damage was observed during re-oxygenation. Tissues responded differentially. GPx and MDA rose in the brain and gills, and SOD (and likely GPx) in the liver during hypoxia. Antioxidants increased further at LOE. Rate of oxygen increase during re-oxygenation did not affect antioxidant responses. In brain and gills, GPx and MDA decreased or recovered after 1-h re-oxygenation. In liver, SOD remained high and GPx increased. In summary, C. abramoides incurred oxidative damage during hypoxic exposure with no additional damage inflicted during re-oxygenation: the rate of re-oxygenation was inconsequential. Literature data support conclusion of greater damage during hypoxia than during re-oxygenation in hypoxia-tolerant fish.
我们研究了在耐缺氧鱼类的低氧或复氧过程中,氧化损伤和抗氧化反应是否更易发生,以及复氧速率是否有影响。设计了一项使用野生捕获的阿氏细脂鲤(巴西内格罗河)的低氧/复氧实验来回答这些问题。在常氧、3小时低氧(2.7 kPa)、3小时低氧后立即或缓慢(3.0 kPa·h)进行1小时或3小时复氧处理后,测量了脑、鳃和肝脏组织中的脂质过氧化(MDA,氧化损伤的指标)以及抗氧化活性(超氧化物歧化酶(SOD)、谷胱甘肽过氧化物酶(GPx)、抗过氧自由基能力(ACAP))。确定了常规耗氧率的临界氧张力(Pcrit)(4.1 kPa)和平衡丧失时的P(LOE)(1.7 kPa),以设定实验性低氧暴露条件。调节指数(衡量随着P下降的氧调节能力)为0.32。低氧期间发生了氧化损伤:复氧期间未观察到额外损伤。各组织反应不同。低氧期间,脑和鳃中的GPx和MDA升高,肝脏中的SOD(可能还有GPx)升高。在平衡丧失时抗氧化剂进一步增加。复氧期间的氧增加速率不影响抗氧化反应。在脑和鳃中,1小时复氧后GPx和MDA下降或恢复。在肝脏中,SOD仍然很高,GPx增加。总之,阿氏细脂鲤在低氧暴露期间遭受了氧化损伤,复氧期间没有额外损伤:复氧速率无关紧要。文献数据支持耐缺氧鱼类在低氧期间比复氧期间损伤更大的结论。