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Bisphenol A-Induced Nephrotoxicity: Mechanistic Insights Into Oxidative Stress, Inflammation, and Cellular Dysfunction.
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This review pulls together existing research showing that BPA, a chemical found in plastics, food packaging, and resins, can damage kidney cells by triggering harmful inflammation and oxidative stress, essentially causing tiny cells to malfunction and die off. Concerningly, common "BPA-free" substitutes like bisphenol F and S appear to cause similar kidney harm, suggesting swapping one plastic chemical for another may not actually be safer. While these findings come mainly from lab and animal studies, they raise real questions about how everyday plastic exposure might affect kidney health over time.
Bisphenol A (BPA), a prevalent endocrine disruptor and component of synthetic resins, has recently gained attention for its nephrotoxic potential. Experimental evidence demonstrates that BPA induces kidney injury through oxidative stress, inflammation, and apoptosis. BPA exposure leads to excessive production of reactive oxygen species, increased lipid peroxidation, and decreased levels of key antioxidant enzymes such as superoxide dismutase, catalase, and glutathione, resulting in redox imbalance. Concurrently, BPA activates inflammatory cytokines, including IL-1β, IL-6, and TNF-α, as well as the NF-κB signaling pathway, which contribute to renal inflammation and tissue injury. Histopathological analyses consistently reveal glomerular congestion, tubular degeneration, and necrosis. In vitro studies further demonstrate reduced renal cell viability and enhanced apoptosis mediated by the activation of PI3K/AKT, Bcl2/Bax-caspase, and AMPK/mTOR signaling pathways. Collectively, these findings highlight BPA's ability to cause both structural and functional damage to the kidney through oxidative and inflammatory cascades. Despite advances in understanding BPA-induced nephrotoxicity, translating experimental findings to human health remains challenging due to interspecies variations, differing exposure routes, and inconsistent epidemiological data. Moreover, growing evidence suggests that BPA substitutes, such as bisphenol F and bisphenol S, possess similar endocrine-disrupting and nephrotoxic effects, raising further safety concerns. Future research should focus on elucidating mechanisms underlying BPA-induced cell cycle arrest, its long-term effects on renal repair, and susceptibility factors such as genetic and sex-specific differences. Addressing these gaps is essential for improving risk assessment and guiding regulatory measures to mitigate BPA-related kidney dysfunction.
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Environmental toxicants and nephrotoxicity: Implications on mechanisms and therapeutic strategies
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This review examines how environmental toxicants, including microplastics, phthalates, and bisphenol A, can damage the kidneys. These substances can accumulate in kidney tissue after being swallowed, inhaled, or absorbed through the skin, triggering inflammation, oxidative stress, and cell death. The findings highlight that the kidneys, which filter about 200 liters of fluid daily, are particularly vulnerable to harm from the growing levels of plastic-related pollutants in our environment.
Micro- and nanoplastics and the kidney: exposure pathways, toxicokinetics, and pathophysiological insights
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Tiny plastic particles from our air, water, and food—called micro- and nanoplastics—can enter our bodies and travel to the kidneys, where studies show they may cause cell damage, inflammation, and scarring over time. This review pulls together existing research on how these plastics get into our system and harm kidney tissue, suggesting that everyday plastic exposure could be an overlooked risk factor for kidney disease. More research is needed, but this is an early signal that reducing plastic exposure might matter for long-term kidney health.
Microplastics and the Kidney: A Narrative Review of Human Evidence, Molecular Mechanisms of Cell Injury, and Future Directions
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This review summarizes existing research on how tiny plastic particles might affect kidney health. It describes how plastics entering cells can trigger stress and damage in lab studies, and notes that human studies have found microplastics in urine and kidney tissue, linked to early signs of kidney damage, though evidence remains limited.
Environmental Nephrotoxicity Across the Life Course: Oxidative Stress Mechanisms and Opportunities for Early Intervention
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This review examines how environmental pollutants, including microplastics, nanoplastics, bisphenol A, and phthalates, can damage kidneys across a person's lifetime, with early-life exposure being particularly concerning. Researchers found that these pollutants promote oxidative stress, inflammation, and epigenetic changes that can program lifelong susceptibility to kidney problems. The study highlights antioxidant-based interventions as a potential strategy for protecting kidney health from environmental contaminant exposure.
Coexposure to microplastic and Bisphenol A exhacerbates damage to human kidney proximal tubular cells
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This study exposed human kidney cells to polyethylene microplastics and bisphenol A (BPA, a common plastic chemical) together and found the combination was significantly more damaging than either substance alone. The co-exposure reduced cell survival and increased both oxidative stress and inflammation in the kidney cells. Since both microplastics and BPA are commonly found in the human body, their combined effect on kidney health is a real concern.
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