Journal of Endocrinology and Reproduction

A. S. Vijayasree ¹, V. Rejitha ¹, Valsa S. Peter ², Oommen V. Oommen ¹, M. C. Subhash Peter ¹

Affiliations
1 Department of Zoology, University of Kerala, Kariavattom, Thiruvananthapuram 695581, IN
2 Department of Zoology, Fatima Mata National College, Kollam 691001, IN

Abstract

The physiological response of climbing perch to water-borne nitrate, an important component of the effluents of coconut husk retting, was examined to identify the mechanism of nitrate tolerance in fish. Indices of interrenal function, and metabolic and osmoregulatory homeostasis were analyzed in fish treated with potassium nitrate. Nitrate loading in water for 48 h produced a significant increase in the plasma cortisol by a low dose (247 μM), whereas a higher dose (494 μM) had little effect. A remarkable cortisol surge was found in the nitrate-treated fish kept for recovery in clean water for 96 h, which correlated with the rise in the plasma Na⁺. Glucose, lactate and Na⁺ concentrations in the plasma showed reduction in the nitrate-exposed fish, whereas plasma urea increased. Nitrate exposure had little influence on the gill and kidney Na⁺, K⁺-ATPase activities but had a stimulatory effect on liver Na⁺, K⁺-ATPase activity, indicating a major role of liver in nitrate tolerance. Overall, the present data indicate that nitrate exposure induces an integrated stress response in climbing perch as a result of an activated interrenal axis and disturbed metabolic and hydromineral regulations. This suggests a protective role of cortisol in the regulation of nitrate tolerance in this fish.

Keywords

^{Anabas testudineus}, Fish, Interrenal, Nitrate, Na⁺, K⁺-ATPase, Metabolism, Osmoregulation, Stress.

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J. Leji ¹, G. S. Babitha ², V. Rejitha ¹, A. S. Vijayasree ¹, J. Ignatius ², V. S. Peter ², O. V. Oommen ¹, M. C. S. Peter ¹

Affiliations
1 Department of Zoology, University of Kerala, Kariavattom, Thiruvananthapuram 695581, Kerala, IN
2 Department of Zoology, Fatima Mata National College, Kollam 695001, Kerala, IN

Abstract

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 PO₄^3- 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.

Keywords

Coconut Husk Retting, Fish, Metabolism, Oreochromis mossambicus, Stress, Thyroid Hormones, Tilapia.

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O. V. Oommen ¹, P. Sreejith ¹, R. S. Beyo ¹, L. Divya ¹, A. S. Vijayasree ¹, M. Manju ¹

Affiliations
1 Department of Zoology, University of Kerala, Kariavattom, Thiruvananthapuram-695 581, Kerala, IN

Abstract

Our studies describe the effect of T₃ on the regulation of mitochondrial metabolism, lipid peroxidation and antioxidant enzyme homeostasis in a fresh water teleost, Anabas testudineus. These experiments suggest the possibility that certain of the clinical and biochemical manifestations of T₃ can be attributed to a direct effect of T₃ on mitochondria. Thyroid hormone enhances mitochondrial ATP production rate in the highly oxidative tissue such as liver. These in vitro and in vivo studies substantiate and confirm the earlier reported T₃-induced oxidative metabolism in lower vertebrates. These induced oxidative metabolisms create oxidative stress in tissues. This confirms that T₃ has an immediate response in in vivo and in vitro system on energy adjustment in the fish, A. testudineus. Tri-iodothyronine is also capable of combating the oxidative stress by activating the antioxidant system to remove the ROS. Tri-iodothyronine appears to have a dual role, as a stimulator of oxidative process and as a regulator of antioxidant enzyme activity. This establishes another example for the multi-functional role of T₃ in lower vertebrates also. However, the precise mechanism of action remains to be understood. The protein expression study revealed that T₃ administration in fish creates hypermetaolic state. This hypermetabolic state creates oxidative stress in fish. To maintain the homeostasis of the fish, physiology the main antioxidant CuZn SOD is directly altered. Due to augmented SOD utilization, expression of CuZn SOD is diminished in fish liver and brain. These findings conclude that thyroid hormone effectively maintains physiological status of fresh water fish. It is obvious that thyroid hormones have an over all effect on metabolism in responsive tissue and that their effect is a direct one. Theses studies establish multi-functional role of T₃ in lower vertebrates.

Keywords

Anabas testudineus, Free Radicals, Mitochondrial Respiration, Superoxide Dismutase, Thyroid Hormone, Tri-Iodothyronine.

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