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Stem cells as sensitive targets of bisphenol-A: a comprehensive review of the effects across multiple populations

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This review pulls together recent research on BPA, a chemical found in plastics, food packaging, and medical devices, showing it can damage stem cells, the body's building blocks for repairing and renewing tissues. Scientists found BPA disrupts how these cells grow, use energy, and communicate, and may even cause changes that affect future generations, especially concerning since BPA often occurs alongside microplastics in our environment. While the findings raise real health concerns, researchers note that studies vary widely in design, so more standardized research is needed before we can fully understand the risk to humans.

Bisphenol A (BPA) remains one of the most extensively studied endocrine-disrupting chemicals, given its ubiquitous presence in everyday materials, ranging from food packaging to medical devices, and the harmful effects on multiple biological systems. Its detection in diverse human biological matrices underscores the clinical relevance of chronic, low-dose exposure. Emerging evidence further indicates that micro- and nanoplastics (MNPs) coexist with BPA in environmental and biological contexts, potentially acting as vectors that amplify exposure-related risks. In this framework, stem cells (SCs) serve as highly sensitive targets and informative models for investigating the biological impact of environmental contaminants, due to their essential role in tissue homeostasis and development. This review systematically evaluates studies published between 2020 and 2026 to characterize the effects of BPA exposure across multiple SC populations, including adipose-derived stem cells, non-adipose mesenchymal stromal cells, embryonic stem cells, induced pluripotent stem cells, neural stem/progenitor cells (NSPCs), and spermatogonial stem cells. Current literature evidence suggests that BPA exposure significantly impairs SC functions, encompassing alterations in lineage commitment, mitochondrial function, oxidative balance, and intercellular communication. Notably, BPA-induced epigenetic dysregulation in germline and pluripotent SCs suggests potential transgenerational effects. Despite the growing body of evidence, significant heterogeneity in experimental models, exposure conditions, and BPA concentrations limits the translation of findings to human health risk assessment. Future research should prioritize standardized exposure protocols, human-relevant models, and exposome-based approaches that account for the complexity of real-world chemical mixtures, including BPA analogs and MNP-associated contaminants.

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