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| Effects of Acute Hypoxia and Reoxygenation on Oxidative Stress in Crucian Carp Carassius auratus |
| ZHANG Qian, HUANG Jinqiang, QUAN Jinqiang, WU Shenji, WANG Xiaolan, PAN Yucai |
| College of Animal Science and Technology, Gansu Agricultural University, Lanzhou 730070, China |
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Abstract Crucian carp Carassius auratus with body weight of (250±10) g was placed in a breeding tank, and exposed to hypoxia [(1.0±0.1) mg/L] maintained by adjusting the amount of injected air and nitrogen for 0 h (control group), 3 h, 6 h, 12 h, and 24 h; after 24 h hypoxia exposure, normal dissolved oxygen level [(6.7±0.1) mg/L] were recovered in 3 h and 6 h and then the oxidative stress indicators of serum and tissue at each time point were measured in crucian carp to evaluate effects of acute hypoxic stress on the oxidative stress of crucian carp. The malondialdehyde content (MDA), activities of superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GSH-Px), and total antioxidant capacity and total protein (TP) levels were shown to be significantly increased in the serum, muscle and gill tissues of crucian carp exposed to acute hypoxic stress (P<0.05). In early reoxygenation, the MDA content and GSH-Px activity in serum and the MDA content in muscle tissue were slightly increased compared to hypoxic stress for 24 h, and the enzyme activities in the remaining tissues decreased significantly in crucian carp (P<0.05) compared to hypoxic stress for 24 h. In 6 h reoxygenation, compared with the control group, except for the fact that the MDA content and CAT activity in muscle were significantly higher than those in the control group (P<0.05), the enzyme activities in other tissues were recovered to the initial value, without significant difference from that in the control group (P>0.05). The findings indicated that crucian carp activated the antioxidant defense system by regulating the activities of antioxidant enzymes in the hypoxic environment, so as to protect the body from oxidative damage caused by hypoxia.
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Received: 24 June 2019
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