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Neuroendocrine indicators of allostatic load reveal impact of environmental acidification in fish.

07:00 EST 30th November 2019 | BioPortfolio

Summary of "Neuroendocrine indicators of allostatic load reveal impact of environmental acidification in fish."

Exposure to environmental contaminants may lead to allostatic load. A situation when the costs of coping with chronic or repeated stress affects long-term survival, reproductive output and, ultimately, ecosystem health. By being a central mediator of behavioral and endocrinal stress responses the brain serotonergic (5-HTergic) system plays a key role in allostatic processes. In this study we explored if sublethal effects of Al in acidified water was reflected in changes in 5-HT neurochemistry and the endocrinal stress response in a unique land-locked salmon from Lake Bygelandsfjorden in southern Norway. Fish were exposed to acidified (pH 5.5) water with different concentrations of Al for five to six days. After this, effects on plasma cortisol levels and telencephalic 5-HT neurochemistry were investigated before and after a standardized acute stress test. In addition, gill Al deposition was investigated to quantify the physiological impact of increasing Al concentrations. Before the stress test, there was a positive dose response relationship between Al concentrations, gill Al deposition, serotonergic turnover rate and plasma cortisol. However, in confinement stressed fish, exposure to the highest Al concentrations (148 μg l) resulted in decreased cortisol values compared to fish exposed lower Al concentrations (74, 94 and 124 μg l). This suggests that fish exposed to the highest Al concentration were unable to mount a proper cortisol response to the confinement and demonstrates that neuroendocrine indicators of allostatic can reveal sublethal effects of acidification and, potentially, environmental impacts of other factors.

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This article was published in the following journal.

Name: Comparative biochemistry and physiology. Toxicology & pharmacology : CBP
ISSN: 1532-0456
Pages: 108679

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