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Polystyrene microplastics induced nephrotoxicity associated with oxidative stress, inflammation, and endoplasmic reticulum stress in juvenile rats
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This study found that polystyrene microplastics caused kidney damage in young rats through a combination of oxidative stress, inflammation, and a cellular stress response called endoplasmic reticulum stress. The microplastics also reduced body weight growth and affected multiple organs including the heart and ovaries. These findings suggest that microplastic exposure during development could be particularly harmful to kidney health in young, growing organisms.
Results revealed that PSMPs noticeably decreased the growth rate of bodyweight, and organ index of the kidney, cardiac, and ovary. The intestinal injury caused by PSMPs exposure was also observed, which was distinctly alleviated with N-acetyl-cysteine (NAC) and Salubrinal (Sal) treatment compared with the single PSMPs group. PSMPs caused histological lesions of the kidney via disrupting the serum blood urea nitrogen (BUN), creatinine (CRE), and pro-inflammatory mediators IL-1β, IL-6, and TNF-α. Furthermore, PSMPs exposure induced ER stress and inflammation presumably potentially mediated by oxidative stress in kidneys of rats. Eventually, PSMPs also promoted renal cells apoptosis, manifested as an obvious increase in the number of positive cells for the dUTP nick end labeling of Terminal deoxynucleotidyl transferase, which also can be confirmed by the elevated expression of genes associated with apoptosis Bcl-2, Bax, Caspase-12, Caspase-9, Caspase-3, and IHC score of Caspase-12 in the PSMPs group. Supplementation of NAC and Sal not only ameliorated the PSMPs-induced oxidative stress and ER stress but also the inflammation and apoptosis in the kidney. Collectively, this study suggested that PSMPs caused nephrotoxicity in juvenile rats potentially through oxidative damage and ER stress, which call for greater efforts to be taken on regulating the PSMPs ingestion in children.
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In an animal study, exposure to polystyrene microplastics built up in the kidneys and caused kidney damage, including harmful oxidative stress, inflammation, and disrupted function of mitochondria, the energy-producing parts of cells. Higher doses caused more buildup and more tissue damage, pointing to the kidney as a key target for microplastic harm.
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Researchers found that polystyrene microplastics caused growth problems and bone damage in young rats by triggering stress in a part of the cell called the endoplasmic reticulum. This stress disrupted the normal process by which cartilage turns into bone in growing animals. The findings raise concerns that microplastic exposure during early development could interfere with normal bone growth in children.
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Researchers used lab-grown kidney organoids made from human stem cells to study how polystyrene microplastics affect kidney development. The microplastics triggered oxidative stress and activated cell death pathways, disrupting the formation of key kidney structures. This study provides direct evidence that microplastic exposure could interfere with human organ development, which is especially concerning for fetuses and young children.
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Tiny plastic particles called nanoplastics, found in everyday items and increasingly in our environment, caused kidney damage in rats by triggering a harmful cell stress response that leads to tissue injury. Researchers found that a drug called 4-PBA (already studied for other health conditions) reversed much of this damage, hinting at a possible way to protect kidneys from plastic pollution exposure. While this study was done in rats, not humans, it adds to growing concerns about how the microplastics and nanoplastics we're exposed to daily might affect our organs over time.
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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.
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