4.7 Article

Maternal exposure to bisphenol S induces neuropeptide signaling dysfunction and oxidative stress in the brain, and abnormal social behaviors in zebrafish (Danio rerio) offspring

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SCIENCE OF THE TOTAL ENVIRONMENT
卷 830, 期 -, 页码 -

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ELSEVIER
DOI: 10.1016/j.scitotenv.2022.154794

关键词

Isotocin; Arginine vasotocin; Social behavior; Anxiety; Enzymatic antioxidant

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Recent studies have found that exposure to bisphenol S (BPS) can have multiple adverse effects on organisms. This study exposed adult female zebrafish to environmentally relevant concentrations of BPS and found that maternal exposure affected the social behavior and anxiety response of male offspring in a dose-specific manner. The impaired social behavior was associated with changes in neuropeptide signaling pathways in the brain.
Recent studies show that bisphenol S (BPS) induces multiple adverse effects in exposed organisms; however, the maternal effects of BPS exposure remain poorly understood. Here, we expose adult female zebrafish to environmentally relevant concentrations of BPS (0, 1, 10, 30 mu g/L) and 1 mu g/L of 17-beta-estradiol (E2) as a positive control for 60 days. Females were then paired with BPS-unexposed males and their offspring were raised in control water for 6 months. Maternal exposure to BPS was found to alter social behavior and anxiety response in a dose-specific manner in male offspring. Group preferences and social cohesion were significantly reduced by maternal exposure to 1 and 10 mu g/L BPS, respectively. Additionally, maternal exposure to 1 and 30 mu g/L BPS and E2 decreased offspring stress responses during the novel tank test. The impaired social behavior was associated with elevated arginine-vasotocin (AVT) level as well as with the altered expression of genes involved in AVT signaling pathway (AVT, avpr1aa) and enzymatic antioxidant genes (cat and Mn-sod) in the brain. Collectively, these results suggest that maternal exposure to environmentally relevant concentrations of BPS alters social behavior in zebrafish offspring, which is likely mediated by oxidative stress and disruption of neuropeptide signaling pathways in the brain.

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