Nitric oxide (NO) is a mediator and biomarker of pro- and anti-inflammatory processes. Excessive levels of NO for long periods have been associated with inflammation and tissue damage. The metabolism and synthesis of NO is usually measured indirectly, as metabolites and enzymes involved in reactions, often as the nitrite/nitrate (NOx) level. The aim of the present study was to measure the NOx levels in vital organs of juvenile silver catfish (Rhamdia quelen) exposed to various levels of eprinomectin in the water. The fish were exposed for 24 and 48h to start concentration (0h) of eprinomectin in water (0.0, 1.12, 1.80, and 3.97μg/L). The eprinomectin concentrations in water were lower at 24h (0.0, 0.85, 1.14, and 1.15μg/L) and 48h (0.0, 0.39, 0.69, and 1.28μg/L), due to the process of eprinomectin metabolization. Subsequently, the fish were left for 48h of recovery in eprinomectin-free water. NO levels were measured indirectly, as NOx levels in brain, liver, and gill tissue. Within 24h of exposure, there was no significant increase in NOx levels in the organs evaluated at any of the concentrations tested. However, increases in NOx levels did occur at 48h of exposure in all organs, particularly at the two highest concentrations of eprinomectin (1.80 and 3.97μg/L). The transfer of fish to eprinomectin-free water did not result in reversal of NOx levels after 48h of recovery, especially in fish that had been exposed to the two highest concentrations in the brain and liver tissues, and for the highest concentration in the gills. We conclude that silver catfish exposed to eprinomectin for up to 48h present possible cerebral, hepatic, and branchial inflammatory process associated with increased tissue NOx levels, and that recovery for 48h in water without antiparasitic is insufficient for the fish to recover from the poisoning.
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