Naphthalene-induced differential tissue damage association with circulating fish phagocyte induction

The effect of naphthalene on phagocytes and associated abnormal cellular activities was studied in Anguilla anguilla L. Fish were exposed to sublethal concentrations (0.1, 0.3, 0.9, 2.7 microM) of naphthalene for 8, 16, 24, 48, and 72 h. Gill, head kidney, and peritoneum phagocyte respiratory burst activity (RBA) was measured by nitroblue tetrazolium reduction assay, whereas lipid peroxidation in fish gill, kidney, and liver was measured by thiobarbituric acid reaction substance. A significant increase (P < 0.05-P < 0.001) in total cell count (TCC) of phagocytes (TCCPH) isolated from gill, head kidney, and peritoneum was observed after 8 h of naphthalene exposure and persisting at 16 h exposure. However, long-term exposures (24, 48, and 72 h) induced a significant (P < 0.05-P < 0.001) decrease in TCC at all the concentration levels. Naphthalene exposure caused a significant (P < 0.05-P < 0.001) RBA induction after 8 and 16 h in gill, head kidney, and peritoneal phagocytes, which consequently resulted in a significant (P < 0.01 and P < 0.001) peroxidative tissue damage increase measured as lipid peroxidation (LPO) in gill, kidney, and liver at the same time intervals. Considering TCCPH, RBA, and LPO, the most affected tissues were gill and kidney after 8 and 16 h exposure to all naphthalene concentrations. RBA was significantly decreased after 24, 48, and 72 h of exposure (P < 0.05-P < 0.001), whereas peroxidative damage increased significantly (P < 0.05-P < 0.001) and persisted in long-term exposures (72 h) at all concentration levels in gill and kidney. Liver short-term exposure (8 and 16 h) to all naphthalene concentrations did not alter LPO activity. Long-term exposures (48 and 72 h) caused a significant (P < 0.01 and P < 0.001) LPO increase, which was more pronounced at 72 h. The results demonstrate that the activation pattern of RBA was corroborated by the extent of phagocyte-induced peroxidative damage in the tissues, as demonstrated by a significant increase of circulating phagocytes. However, the route of exposure and mode of entry of a pollutant may affect the activation pattern of circulating fish phagocytes. It is proposed that measurement of phagocyte-induced reactive oxygen species and their association with peroxidative damage in fish tissues may prove to be useful in biomonitoring fish exposure to aquatic pollutants.