PUBLICATION

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

Authors
Salahinejad, A., Attaran, A., Meuthen, D., Rachamalla, M., Chivers, D.P., Niyogi, S.
ID
ZDB-PUB-220329-9
Date
2022
Source
The Science of the total environment   830: 154794 (Journal)
Registered Authors
Rachamalla, Mahesh
Keywords
Anxiety, Arginine vasotocin, Enzymatic antioxidant, Isotocin, Social behavior
MeSH Terms
  • Animals
  • Brain/metabolism
  • Female
  • Humans
  • Male
  • Maternal Exposure/adverse effects
  • Neuropeptides*/metabolism
  • Oxidative Stress
  • Phenols
  • Signal Transduction
  • Social Behavior
  • Sulfones
  • Zebrafish*/physiology
PubMed
35341835 Full text @ Sci. Total Environ.
Abstract
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 μg/L) and 1 μg/L of 17-β-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 μg/L BPS, respectively. Additionally, maternal exposure to 1 and 30 μg/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.
Genes / Markers
Figures
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Antibodies
Orthology
Engineered Foreign Genes
Mapping