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 fish 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.

Arsenic (As) is a poisonous metalloid that is toxic to both humans and animals. Drinking water contamination has been linked to the development of cancer (skin, lung, urinary bladder, and liver), as well as other disorders such as diabetes and cardiovascular, gastrointestinal, neurological, and developmental damage. According to epidemiological studies, As contributes to male infertility, sexual dysfunction, poor sperm quality, and developmental consequences such as low birth weight, spontaneous abortion, and small for gestational age (SGA). Arsenic exposure negatively affected male reproductive systems by lowering testicular and accessory organ weights, and sperm counts, increasing sperm abnormalities and causing apoptotic cell death in Leydig and Sertoli cells, which resulted in decreased testosterone synthesis. Furthermore, during male reproductive toxicity, several molecular signalling pathways, such as apoptosis, inflammation, and autophagy are involved. Phytonutrient intervention in arsenic-induced male reproductive toxicity in various species has received a lot of attention over the years. The current review provides an in-depth summary of the available literature on arsenic-induced male toxicity, as well as therapeutic approaches and future directions.

The reproductive consequences of environmentally relevant trophic exposure to arsenic in fish are poorly understood, despite diet being the major exposure source in many contaminated systems. This study investigated the reproductive effects of chronic dietary exposure to arsenic in adult Zebrafish via arsenic-contaminated oligochaete (Lumbriculus variegatus) worms. Worms pre-exposed to arsenite (0, 2.5, and 5.0 mg/L) for 14 days resulted in arsenic body burdens of 0.25 (Control), 34.69 (Low), and 77.79 (High) μg/g dry weight. Zebrafish were fed these worms at 3.5 % of body weight twice daily for 60 days. Reproductive endpoints assessed included gonadosomatic index (GSI), hepatosomatic index (HSI), fecundity, fertilization rate, and mating behaviour. Brain, liver, gonads, and blood plasma were assessed for gene expressions related to hypothalamus-pituitary-gonadal (HPG) axis genes, oxidative damage in hepatic and gonadal tissues, and to quantify the circulating 17β-estradiol (E2), 11-keto testosterone (11KT), and vitellogenin (VTG) levels in males and females. Sperm density and motility were assessed in males, and gonadal histopathology was conducted in both sexes. Dose-dependent reductions in GSI, HSI, fecundity, fertilization rate, and mating behaviour were recorded, along with oxidative damage in gonadal and liver tissues. Arsenic also reduced sperm quality and decreased the proportion of mature gametes in both ovaries and testes. Chronic exposure significantly altered HPG axis gene expression and disrupted circulating E2, 11-KT, and VTG levels in both sexes. Overall, these findings provide novel mechanistic insights into arsenic-induced reproductive toxicity in fish, which have important implications for understanding the consequences of arsenic contamination in aquatic ecosystems.