Hypoxia and recovery perturb free radical processes and antioxidant potential in common carp (Cyprinus carpio) tissues
The effects of hypoxia exposure and subsequent normoxic recovery on the levels of lipid peroxides (LOOH), thiobarbituric acid reactive substances (TBARS), carbonylproteins, total glutathione levels, and the activities of six antioxidant enzymes were measured in brain, liver, kidney and skeletal muscle of the common carp Cyprinus carpio. Hypoxia exposure (25% of normal oxygen level) for 5 h generally decreased the levels of oxidative damage products, but in liver TBARS content were elevated. Hypoxia stimulated increases in the activities of catalase (by 1.7-fold) and glutathione peroxidase (GPx) (by 1.3-fold) in brain supporting the idea that anticipatory preparation takes place in order to deal with the oxidative stress that will occur during reoxygenation. In liver, only GPx activity was reduced under hypoxia and reoxygenation while other enzymes were unaffected. Kidney showed decreased activity of GPx under aerobic recovery but superoxide dismutase (SOD) and catalase responded with sharp increases in activities. Skeletal muscle showed minor changes with a reduction in GPx activity under hypoxia exposure and an increase in SOD activity under recovery. Responses by antioxidant defenses in carp organs appear to include preparatory increases during hypoxia by some antioxidant enzymes in brain but a more direct response to oxidative insult during recovery appears to trigger enzyme responses in kidney and skeletal muscle.
|Keywords||Antioxidant enzymes, Carbonylproteins, Common carp, Hypoxia, Oxidative stress|
|Journal||International Journal of Biochemistry and Cell Biology|
Lushchak, V.I. (Volodymyr I.), Bagnyukova, T.V. (Tetyana V.), Lushchak, O.V. (Oleh V.), Storey, J, & Storey, K. (2005). Hypoxia and recovery perturb free radical processes and antioxidant potential in common carp (Cyprinus carpio) tissues. International Journal of Biochemistry and Cell Biology, 37(6), 1319–1330. doi:10.1016/j.biocel.2005.01.006