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Article Abstract

Arsenic is a known reproductive toxicant to fish; however, the persistence of its toxicity beyond the parental generation remains unclear. The present study investigated the effects of maternal and paternal arsenic exposure via diet on the reproduction and development of zebrafish offspring. Adult male zebrafish exposed to dietary arsenic [30, 60 or 100 μg/g as arsenite for 90 days; F generation] were crossed with unexposed (control) females and vice versa to generate F progeny of maternal (ME) and paternal (PE) arsenic exposures, respectively. F larvae were raised to adulthood in clean water and diet, and males and females from respective ME and PE groups were then bred to evaluate the reproductive and developmental effects of parental arsenic exposure in the offspring generations. A significant reduction in fecundity, fertilization success, and larval (F) development was observed with ME to arsenic, even at the lowest dose. However, similar effects were only recorded with PE to arsenic at medium and high doses. In addition, the HPG axis genes were consistently downregulated in F males and females of both ME and PE treatment groups. The circulating E2 and VTG levels were also decreased in F females of the ME treatment groups, whereas the circulating 11-KT levels were reduced in F males of both the ME and PE treatment groups. In general, dysregulation of the HPG axis was more sensitive to the ME than the PE. In addition, arsenic exposure induced hypermethylation of the promoter region of key HPG axis genes, notably sf-1 in the brain and cyp19a1a in the gonads in both males and females of F and F generations of maternal and paternal arsenic lineages. Overall, our study demonstrated that both maternal and paternal arsenic exposure causes reproductive and developmental toxicity in zebrafish offspring, likely by disrupting the HPG axis via epigenetic alterations.

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http://dx.doi.org/10.1016/j.envpol.2025.126528DOI Listing

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