Abstract

We examined the effects of carbaryl (1-naphthyl methylcarbamate; sevin), a carbamate pesticide, on interrenal and thyroid activities and mitochondrial rich (MR) cell function in climbing perch to understand the physiological basis of toxicity acclimation in this fish to the chemical stressor. Carbaryl exposure (5–20mgL−1) for 48h increased cortisol and glucose, but decreased the T3 level without affecting T4 concentration in the plasma. These responses of the carbaryl-exposed fish were nullified and a rise in plasma T4 occurred in these fish when they were kept for 96h recovery in clean water. A tight plasma mineral control was indicated in the carbaryl-exposed fish as reflected by the unchanged plasma Na, K, Ca and inorganic phosphate levels. The ouabain-sensitive Na+, K+-ATPase activity showed an increase in the gills but the intestinal and renal tissues showed little response to carbaryl treatment. However, substantial increases in the intestinal and renal Na+, K+-ATPase activities occurred in the recovery fish. The MR cells in the branchial epithelia showed a strong Na+, K+-ATPase immunoreactivity to carbaryl treatment indicating an activated MR cell function. The numerical MR cell density remained unchanged, but stretching of secondary gill lamellae as part of gill remodeling occurred during carbaryl exposure. The increased surface of these lamellae with abundant MR cells as a result of its migration into the lamellar surface points to marked structural and functional modifications of these cells in the carbaryl-treated fish which is likely to a target for carbaryl action. The rise in plasma T4 and the restoration of normal branchial epithelia in the recovery fish indicate a thyroidal involvement in the recovery response and survival. Our data thus provide evidence that carbaryl exposure and its recovery evoke interrenal and thyroid disruption in this fish leading to a modified osmotic response including an altered MR cell function.

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