In vitro exposure to polystyrene microplastic induces oxidative stress mediated β-cell dysfunction.

Environmental pollution has emerged as a major global health concern, with microplastics (MPs) now recognized as pervasive contaminants in the ecosystem and human tissues. Among them, polystyrene microplastics (PS-MPs) is frequently detected in metabolically relevant organs, raising concerns regarding their roles in diabetes development. In this study, we investigated the cellular and functional effects of PS-MP exposure in pancreatic β-cells using the MIN6 cell line. Our results demonstrated that 1 μm PS-MPs were efficiently internalized and predominantly localized within cytoplasmic and perinuclear regions of the cells. Exposure to PS-MP induced a dose- and time-dependent increase in mitochondrial superoxide and intracellular reactive oxygen species, accompanied by significant suppression of functional β-cell markers. This oxidative stress was associated with pronounced necrotic cell death. Moreover, metabolic viability assays revealed a progressive decline in β-cell viability along with suppression of key β-cell identity markers, including PDX1 and MAFA. Collectively, these alterations contributed to early β-cell dysfunction, a hallmark event in the initiation of diabetes. To our knowledge, this study is among the first to demonstrate an association between PS-MPs exposure, oxidative stress-mediated cytotoxicity, necrosis, and functional impairment in pancreatic β-cells. Our findings highlight a plausible environmental route linking chronic microplastic exposure to β-cell dysfunction, impaired insulin production, and heightened susceptibility to diabetes, underscoring the urgent need to evaluate microplastics as emerging metabolic disruptors.