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Using acs-22 mutant Caenorhabditis elegans to detect the toxicity of nanopolystyrene particles
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Researchers used C. elegans worms with a defective intestinal barrier to show that nanoplastics at environmentally predicted concentrations (1 µg/L) can translocate to internal organs and activate oxidative stress pathways when the gut barrier is compromised — suggesting susceptibility may increase under certain disease conditions.
In this study, we employed Caenorhabditis elegans with acs-22 mutation to examine the in vivo effect of functional deficit in intestinal barrier on toxicity and translocation of nanopolystyrene particles. Mutation of acs-22 leads to deficit in intestinal barrier. After prolonged exposure, nanopolystyrene particles at concentrations ≥1 μg/L could cause toxicity on acs-22 mutant nematodes. acs-22 mutation resulted in translocation of nanopolystyrene particles into targeted organs through intestinal barrier in nanopolystyrene particles (1 μg/L) exposed nematodes. After prolonged exposure, nanopolystyrene particles (1 μg/L) dysregulated expressions of some genes required for the control of oxidative stress and activated expression of Nrf signaling pathway. Therefore, under certain pathological conditions, our results suggest the potential toxicity of nanoplastic particles at predicted environmental concentration on organisms after long-term exposure.
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