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Metabolic and osmoregulatory responses of the sea bass Lates calcarifer to nitrite exposure



Metabolic and osmoregulatory responses of the sea bass Lates calcarifer to nitrite exposure



Environmental Toxicology & Water Quality 12(3): 257-264



Sea bass (Lates calcarifer) were exposed to seawater containing 0, 30, 50, or 80 mg L-1 NO-2-N for 4 days, and changes in metabolite levels and enzyme activities were assessed. Distinct signs of osmoregulatory dysfunction were evident in nitrite-exposed fish as serum Na+ and Cl- levels were elevated and branchial Na+-K+-ATPase activity was significantly reduced. Serum lactate and protein levels were significantly elevated and lowered respectively only at the highest nitrite level (80 mg L-1 NO-2-N). Significantly increased serum ammonia and urea and decreased serum glucose and liver glycogen levels were evident also at lower nitrite levels. Liver water, liver protein and lactate, brain and muscle lactate, and muscle water content were unaffected. In the liver, significant decreases were observed for the activities of glycogen phosphorylase a, glutamate-oxaloacetate transaminase, and glutamate dehydrogenase, but the activities of lactate dehydrogenase, isocitrate dehydrogenase, glucose-6-phosphatase, glutamate pyruvate transaminase, and glucose-6-phosphate dehydrogenase were unaffected. While ATP, ADP, and AMP levels were all lowered in nitrite-exposed fish, the adenylate energy charge was maintained at fairly constant level. By producing ammonia via the degradation of AMP to IMP, stabilization of the adenylate energy charge can be achieved. It is postulated that this event probably represents an adaptive strategy employed by the sea bass to counteract nitrite toxicity.

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Accession: 003199311

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DOI: 10.1002/(sici)1098-2256(1997)12:3<257::aid-tox9>3.0.co;2-7


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