Annali dell'Istituto superiore di sanita · 2026
Bisphenol S-induced inflammation: a comparative insight on inflammatory pathway activation in zebrafish and rodent models.
СтатьяОбзорСравнительное исследованиеНазвание и аннотация: Перевод в очереди
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Wan Azhan Wan Nur Izzati, Zakaria Fatin Nadzirah, Al' Arifin Danial Akmal Fuad, Amlie Nur-Zulaikha, Kamarudin Evana, Paiman Faheze, Risandiansyah Rio, Dasiman Razif
Аннотация
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.
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.