Thyroidal and Osmoregulatory Responses in Tilapia (Oreochromis mossambicus) to the Effluents of Coconut Husk Retting
The coconut husk retting in the backwaters of Kerala in Southern India, releases toxic effluents (CHRE), which pose a threat to the life of many inhabitants including fish. The indices of osmoregulatory activity and the levels of plasma triiodothyronine (T3) and thyroxine (T4) in the Mozambique tilapia Oreochromis mossambicus were quantified after exposing them to the effluents to understand the physiological mechanism of tolerance. The plasma glucose, an indicator of catecholamine secretion, remained unchanged in the tilapia exposed to CHRE. The plasma T4 significantly increased in the tilapia kept in CHRE-rich water, though it declined in the fish kept for recovery in lake water. The plasma K+ significantly decreased in the tilapia treated with CHRE, which returned to the basal levels in those kept for recovery. The Na+, Ca2+ and PO43- remained the same in both treated and untreated fish. The branchial Na+, K+-ATPase activity increased in the CHRE-exposed fish, and such an effect was not reversed in the recovery group. The renal Na+, K+-ATPase activity decreased in the lake water-exposed tilapia but not in the CHRE-treated fish. A reversal in the renal Na+, K+-ATPase activity was obtained in the tilapia kept for recovery in lake water. The intestinal Na+, K+-ATPase activity significantly declined in the CHRE-exposed tilapia but not in the recovery group. The data indicate that the presence of CHRE in lake water affects the osmoregulatory potential of tilapia without influencing their metabolic status. The up-regulated thyroid activity in the CHRE-exposed tilapia points to its involvement in the ion homeostasis during CHRE intoxication.
Coconut Husk Retting, Fish, Metabolism, Oreochromis mossambicus, Stress, Thyroid Hormones, Tilapia.
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