Bisphenol S-induced inflammation: a comparative insight on inflammatory pathway activation in zebrafish and rodent models.

BACKGROUND

Bisphenol S (BPS) is a widespread BPA substitute with emerging immunotoxicity; this review synthesizes zebrafish and rodent experimental evidence to clarify BPS-induced inflammation.

METHODS

Narrative synthesis of experimental studies in zebrafish and rodent models, focusing on molecular pathways, organ-level effects, and exposure timing.

RESULTS

Across models, BPS consistently activates an oxidative stress-mediated NF-κB axis with increased ROS, lipid peroxidation, and upregulation of TNF-α, IL-1β, and IL-6; chronic and developmental low-to-moderate exposures produced stronger inflammatory phenotypes than acute high doses.

CONCLUSIONS

Convergent mechanistic and pathological findings strengthen the weight of evidence for BPS immunotoxicity and support targeted monitoring and controls; key research gaps include inflammasome activation, receptor mechanisms, sex differences, mixture effects, epigenetic regulation, and standardization.