Selenium toxicity in fishes: A current perspective.

Anthropogenic activities have led to increased levels of contaminants that pose significant threats to aquatic organisms, particularly fishes. One such contaminant is Selenium (Se), a metalloid which is released by various industrial activities including mining and fossil fuel combustion. Selenium is crucial for various physiological functions, however it can bioaccumulate and become toxic at elevated concentrations. Given that fishes are key predators in aquatic ecosystems and a major protein source for humans, Se accumulation raises considerable ecological and food safety concerns. Selenium induces toxicity at the cellular level by disrupting the balance between reactive oxygen species (ROS) production and antioxidant capacity leading to oxidative damage. Chronic exposure to elevated Se impairs a wide range of critical physiological functions including metabolism, growth and reproduction. Selenium is also a potent teratogen and induces various types of adverse developmental effects in fishes, mainly due to its maternal transfer to the eggs. Moreover, that can persist across generations. Furthermore, Se-induced oxidative stress in the brain is a major driver of its neurotoxicity, which leads to impairment of several ecologically important behaviours in fishes including cognition and memory functions, social preference and interactions, and anxiety response. Our review provides an up-to-date and in-depth analysis of the various adverse physiological effects of Se in fishes, while identifying knowledge gaps that need to be addressed in future research for greater insights into the impact of Se in aquatic ecosystems.
Competing Interests: Declaration of competing interest The authors declare the following financial interests/personal relationships which may be considered as potential competing interests:MD HELAL UDDIN reports was provided by University of Saskatchewan. If there are other authors, they declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.
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