We can't find the internet
Attempting to reconnect
Something went wrong!
Hang in there while we get back on track
Environmental Nephrotoxicity Across the Life Course: Oxidative Stress Mechanisms and Opportunities for Early Intervention
AI summary Read the abstract
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.
Chronic kidney disease (CKD) affects nearly 10% of the global population, ranks among the top ten causes of death, and often progresses silently to end-stage disease without timely intervention. Increasing evidence indicates that many adult-onset cases originate in early life through adverse influences on kidney development, a process termed kidney programming within the Developmental Origins of Health and Disease (DOHaD) framework. Environmental pollutants are now recognized as key drivers of kidney injury across the life course. Heavy metals, air pollutants, plastic contaminants such as bisphenol A, phthalates, and micro/nanoplastics-as well as biocontaminants like mycotoxins and aristolochic acid-and chronic light pollution can accumulate in kidney tissue or act systemically to impair function. These exposures promote oxidative stress, inflammation, and endothelial and circadian disruption, culminating in tubular injury, glomerular damage, and fibrosis. Notably, early-life exposures can induce epigenetic modifications that program lifelong susceptibility to CKD and related complications. Oxidative stress is central to these effects, mediating DNA, lipid, and protein damage while influencing developmental reprogramming during gestation. Preclinical studies demonstrate that antioxidant-based interventions may mitigate these processes, providing both renoprotective and reprogramming benefits. This review explores the mechanistic links between environmental pollutants, oxidative stress, and kidney disease and highlights antioxidant strategies as promising avenues for prevention and intervention in vulnerable populations.
More Papers Like This
Environmental toxicants and nephrotoxicity: Implications on mechanisms and therapeutic strategies
AI summary Read the abstract
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
AI summary Read the abstract
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.
From exposure to injury: signaling mechanisms of microplastic-induced renal toxicity: an extensive review
AI summary Read the abstract
Researchers reviewed experimental and mechanistic evidence on how micro- and nanoplastics damage kidneys, synthesizing a framework in which oxidative stress, inflammasome activation, mitochondrial dysfunction, and profibrotic remodeling collectively drive nephron injury — while noting that standardized biomonitoring protocols and nanoscale detection methods remain critical unresolved challenges.
Bisphenol A-Induced Nephrotoxicity: Mechanistic Insights Into Oxidative Stress, Inflammation, and Cellular Dysfunction.
AI summary Read the abstract
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.
Polyethylene microplastics disrupt renal function, mitochondrial bioenergetics, redox homeostasis, and histoarchitecture in Wistar rats
AI summary Read the abstract
Researchers gave rats polyethylene microplastics orally for 28 days and found dose-dependent kidney damage, including impaired filtration, electrolyte imbalances, and tissue inflammation. The microplastics depleted antioxidant defenses, increased oxidative stress markers, and disrupted mitochondrial energy production in kidney cells, identifying the kidneys as a critical target of microplastic toxicity.
Research digests by email
When a large batch of papers lands in the Atlas, we read through it and send a short write-up of what stood out.