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Disruption of the melatonin rhythm in wild and farmed fish: a consequence of prolonged thyroxine administration and calcium depletion

Identifieur interne : 001088 ( Main/Exploration ); précédent : 001087; suivant : 001089

Disruption of the melatonin rhythm in wild and farmed fish: a consequence of prolonged thyroxine administration and calcium depletion

Auteurs : E. Kulczykowska [Pologne] ; E. Sokolowska [Pologne] ; M. Gozdowska [Pologne] ; H. Kalamarz [Pologne]

Source :

RBID : ISTEX:C45492DE85B650EA9CEA4904C5F61C408D5C607F

Abstract

Recent studies suggest that the pineal gland and its major product melatonin (N‐acetyl‐5‐methoxytryptamine: Mel) play a role in integration of various neural and endocrine functions. Observations indicate that Mel as a signal of photoperiod regulates a number of biological phenomena, including reproduction, day/night activity and many other physiological events associated with daily or seasonal rhythms in vertebrates, including fish. Mel has also been found to be a highly effective preventive antioxidant and free radical scavenger, protecting organism from oxidative damage. In all species examined, plasma melatonin concentration shows a diurnal rhythm, with the highest levels during the night. Our studies are focused on the cues affecting Mel synthesis capacity in wild and farmed fish. The Mel rhythm in fish can be disrupted by fluctuations in surrounding calcium concentration or by prolonged thyroxine (T4) exposure. Physiological depletion of plasma ionized calcium may limit the capacity of Mel night production in two fish species, farmed rainbow trout and wild flounder. Prolonged (2 week) exposure to high level of exogenous thyroxine (T4) results in reduced night‐time plasma Mel levels, and may thus inhibit the melatonin‐related time‐keeping system in juvenile salmon. Disruption of the daily Mel rhythm implies a reduced ability of organisms to respond properly to environmental signals, and may be a useful indicator of disturbance in physiological functions.

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DOI: 10.1111/j.0022-1112.2004.559ao.x


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