Reduced enzymatic antioxidative defense in deep-sea fish.
نویسندگان
چکیده
Oxygen, while being an obligate fuel for aerobic life, has been shown to be toxic through its deleterious reactive species, which can cause oxidative stress and lead ultimately to cell and organism death. In marine organisms, reactive oxygen species (ROS), such as the superoxide anion and hydrogen peroxide, are generated within respiring cells and tissues and also by photochemical processes in sea water. Considering both the reduced metabolic rate of nektonic organisms thriving in the deep sea and the physico-chemical conditions of this dark, poorly oxygenated environment, the meso- and bathypelagic waters of the oceans might be considered as refuges against oxidative dangers. This hypothesis prompted us to investigate the activities of the three essential enzymes (superoxide dismutase, SOD; catalase, CAT; glutathione peroxidase, GPX) constitutive of the antioxidative arsenal of cells in the tissues of 16 species of meso- and bathypelagic fishes occurring between the surface and a depth of 1300 m. While enzymatic activities were detected in all tissues from all species, the levels of SOD and GPX decreased in parallel with the exponential reduction in the metabolic activity as estimated by citrate synthase activity. In contrast, CAT was affected neither by the metabolic activity nor by the depth of occurrence of the fishes. High levels of metabolic and antioxidative enzymes were detected in the light organs of bioluminescent species. The adjustment of the activity of SOD and GPX to the decreased metabolic activity associated with deep-sea living suggests that these antioxidative defense mechanisms are used primarily against metabolically produced ROS, whereas the maintenance of CAT activity throughout all depths could be indicative of another role. The possible reasons for the occurrence of such a reduced antioxidative arsenal in deep-sea species are discussed.
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ورودعنوان ژورنال:
- The Journal of experimental biology
دوره 203 Pt 24 شماره
صفحات -
تاریخ انتشار 2000