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Polystyrene nanoplastics exacerbate gentamicin-induced nephrotoxicity in adult rat by activating oxidative stress, inflammation and apoptosis pathways
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Researchers co-exposed rats to polystyrene nanoplastics and the antibiotic gentamicin and found that the combination caused significantly greater kidney damage than either substance alone, amplifying oxidative stress, inflammation, and mitochondrial apoptosis in a synergistic manner.
Nanoplastics (NPs) and pharmaceutical residues are environmental pollutants that can bioaccumulate in the food chain, thus increasing the risk of harmful effects due to concomitant exposure in both humans and animals. However, the impact of such co-exposure on target tissue toxicity and mechanism remains unclear. In this study, we aimed to investigate the effect of combined exposure to widespread polystyrene NP (Ps-NP) contaminant and a widely used antibiotic, gentamicin (GEN) on nephrotoxicity in adult rat. A total of 40 male Wistar rats were assigned into four groups; control group (C), GEN exposed-group (100 mg/kg/day, i.p.), Ps-NPs exposed-group (2.5 mg/kg/day, orally) and co-exposure-group (100 mg Ps-NPs/kg/day orally + 2.6 mg GEN/kg/day i.p.) for 15 consecutive days. Kidneys were excised at sacrifice on day 15 for the examination of: (i) renal function parameters and renal oxidative stress (oxidant and antioxidant markers); (ii) mRNA expression of key regulators of oxidative stress and inflammation response (NF-κB, TNF-α, IL-6 and NRF-2) and mitochondrial apoptosis pathway (Bax, Bcl-2, caspase-9 and caspase-3); (iii) histopathology. Levels of urea and creatinine in serum of NPs or/and GEN-treated rats were significantly increased with marked histopathological changes in the kidney. Additionally, the oxidative stress markers (MDA, PCO and NO) were increased with a decrease of antioxidant enzyme activities. Furthermore, Ps-NPs or/and GEN-treated rats exhibited increased expression of mRNA related to oxidative stress (NRF-2), inflammation (TNF-α, IL-6) and apoptosis (Bax, Bcl-2, caspase-9 and caspase-3). Our results revealed that co-exposure of adult rats to Ps-NPs and GEN had a synergic-adverse effect on the kidney function. This study highlights a new finding regarding the combined toxicity of NPs and pharmaceutical pollutants on kidney function, suggesting potential synergistic interaction between these substances.
More Papers Like This
Combined Exposure to Polystyrene Nanoplastics and Gentamicin Promotes Liver Toxicity Through Oxidative Stress, Inflammation and Apoptotic Pathways: In Vivo and In Silico Studies
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Scientists found that when rats were exposed to tiny plastic particles (nanoplastics) together with a common antibiotic called gentamicin, their livers showed more damage than exposure to either one alone—including increased stress, inflammation, and cell death in liver tissue. This matters because it suggests that everyday exposure to plastic pollution might make certain medications more harmful to our organs, though more research is needed to confirm this happens in humans too.
Combined exposure to polystyrene nanoplastics and bisphenol A results in mitochondrial damage and ferroptosis via the PI3K-AKT signaling pathway in mice kidneys
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Researchers exposed mice to polystyrene nanoplastics combined with bisphenol A for six weeks and found that co-exposure caused significant kidney damage through mitochondrial dysfunction and a form of cell death called ferroptosis. The combined exposure was more harmful than either contaminant alone, operating through the PI3K-AKT signaling pathway. The findings suggest that nanoplastics acting as carriers for co-pollutants like BPA may amplify toxic effects on kidney tissue.
Exploring the Mechanismof Kidney Injury in Mice Inducedby High-Fat Diet and Polystyrene Nanoplastics Co-Exposure Throughthe Kidney-Gut Axis
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This mouse study found that combining a high-fat diet with polystyrene nanoplastic exposure (100 nm, 25 mg/kg/day) worsened kidney toxicity beyond high-fat diet alone, with the combination disrupting lipid metabolism via tryptophan and glycerophospholipid pathways and exacerbating gut microbiota dysbiosis through the kidney-gut axis.
Aging amplifies the combined toxic effects of polystyrene nanoplastics and norfloxacin on human intestinal cells
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Researchers investigated how environmental aging of polystyrene nanoplastics affects their combined toxicity with the antibiotic norfloxacin on human intestinal cells. They found that aged nanoplastics were taken up more readily by cells and significantly amplified the harmful effects of the antibiotic, including increased cell damage. The study suggests that weathered nanoplastics in the environment may pose greater health risks than fresh particles, especially when combined with other contaminants.
Issue Information‐ToC
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This brief notice indicates a paper in the journal issue that examines how polystyrene nanoplastics worsen inflammation-triggered cell death (apoptosis) in mouse kidney cells exposed to bacterial toxins. The interaction between nanoplastics and inflammatory signals may amplify kidney damage beyond what either stressor alone would cause.
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