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Polystyrene nanoplastics exacerbated Pb-induced liver toxicity in mice
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Researchers found that polystyrene nanoplastics exacerbated lead-induced liver toxicity in mice, with co-exposure causing higher lead accumulation, more severe inflammation, increased oxidative stress, and greater disruption of protective Nrf2 signaling pathways compared to lead alone.
Nanoplastics are widely distributed in the environment and can adsorb heavy metals, which poses a potential threat to human health through food chain. It is necessary to assess the combined toxicity of nanoplastics and heavy metals. The adverse effect of Pb and nanoplastics on liver, single or in combination, was evaluated in this study. The results showed that the Pb content in co-exposure group of nanoplastics and Pb (PN group) was higher than the group exposed to Pb alone (Pb group). And more severe inflammatory infiltration was observed in liver sections of PN group. The level of inflammatory cytokines and malondialdehyde were increased, while the superoxide dismutase activity was decreased in liver tissues of PN group. Moreover, the gene expression level of nuclear factor-erythroid 2-related factor 2, nicotinamide adenine dinucleotide phosphate:quinine oxidoreductase 1 and catalase, which is related to antioxidation, was downregulated. And the expression level of cleaved-Caspase9 and cleaved-Caspase3 were increased. However, with the supplementation of oxidative stress inhibitor N-Acetyl-L-cysteine, liver damage shown in PN group was evidently alleviated. In summary, nanoplastics evidently exacerbated the deposition of Pb in liver and potentially aggravated the Pb-induced liver toxicity by activating oxidative stress.
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Polystyrene nanoplastics potentiate the development of hepatic fibrosis in high fat diet fed mice
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Researchers found that polystyrene nanoplastics worsened liver damage in mice fed a high-fat diet by increasing oxidative stress, inflammation, and the infiltration of immune cells in liver tissue. The nanoplastic exposure accelerated the progression from fatty liver to hepatic fibrosis in the diet-induced model. The study suggests that nanoplastic exposure may compound the health risks associated with metabolic conditions affecting the liver.
Exposure to polystyrene nanoplastics induces hepatotoxicity involving NRF2-NLRP3 signaling pathway in mice
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Mice and cultured liver cells were exposed to 20 nanometer polystyrene nanoplastics. The particles raised reactive oxygen species, suppressed the NRF2 antioxidant pathway and increased inflammatory signaling in the liver. Activating NRF2 with the compound tert-butylhydroquinone reduced the oxidative stress.
Combined exposure of nano‐titanium dioxide and polystyrene nanoplastics exacerbate oxidative stress‐induced liver injury in mice by regulating the Keap‐1 / Nrf2 / ARE pathway
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Researchers found that mice exposed to both polystyrene nanoplastics and nano-titanium dioxide together suffered worse liver damage than those exposed to either substance alone. The combined exposure amplified oxidative stress and disrupted a key protective signaling pathway in the liver, suggesting that co-exposure to multiple nanoparticles may pose greater health risks than individual exposures.
Polystyrene nanoplastics exacerbate aflatoxin B1-induced hepatic injuries by modulating the gut−liver axis
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Mice exposed to both polystyrene nanoplastics and aflatoxin B1, a common food contaminant from mold, suffered worse liver damage than from either pollutant alone. The nanoplastics disrupted gut bacteria and weakened the intestinal barrier, allowing more toxins to reach the liver through the gut-liver axis. This study is concerning because it shows that microplastics can amplify the harmful effects of other food contaminants people are already exposed to.
Combined effect of arsenic and polystyrene-nanoplastics at environmentally relevant concentrations in mice liver: Activation of apoptosis, pyroptosis and excessive autophagy
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Researchers investigated the combined toxic effects of arsenic and polystyrene nanoplastics on mouse liver at environmentally relevant concentrations. The study found that co-exposure activated multiple cell death pathways including apoptosis, pyroptosis, and excessive autophagy in liver tissue, suggesting that the interaction between nanoplastics and heavy metals may amplify liver damage.
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