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Article ? AI-assigned paper type based on the abstract. Classification may not be perfect — flag errors using the feedback button. Tier 2 ? Original research — experimental, observational, or case-control study. Direct primary evidence. Gut & Microbiome Human Health Effects Nanoplastics Reproductive & Development Sign in to save

Exposure to epoxy-modified nanoplastics in the range of μg/L causes dysregulated intestinal permeability, reproductive capacity, and mitochondrial homeostasis by affecting antioxidant system in Caenorhabditis elegans

Aquatic Toxicology 2023 10 citations ? Citation count from OpenAlex, updated daily. May differ slightly from the publisher's own count. Score: 50 ? 0–100 AI score estimating relevance to the microplastics field. Papers below 30 are filtered from public browse.
Man Qu Qinlin Wu, Man Qu Man Qu Man Qu Man Qu Man Qu Man Qu Man Qu Man Qu Man Qu Man Qu Man Qu Yuhan An, Man Qu Long Miao, Yuhan An, Xinyi Jiang, Man Qu Man Qu Man Qu Xing Zhang, Xing Zhang, Xinyi Jiang, Qinlin Wu, Xing Zhang, Xing Zhang, Long Miao, Qinlin Wu, Yuhan An, Xing Zhang, Yuhan An, Xing Zhang, Yang Wang, Yuhan An, Yang Wang, Yuhan An, Xinyi Jiang, Long Miao, Man Qu Man Qu

Summary

Researchers found that epoxy-modified nanoplastics caused toxic effects in the model organism C. elegans at concentrations as low as 1 microgram per liter, including reduced locomotion, increased intestinal permeability, and impaired reproductive capacity. The study suggests that surface chemical modifications can significantly enhance the toxicity of nanoplastics by disrupting antioxidant defense systems and mitochondrial function.

Polymers
Body Systems

Although surface chemically modified nanopolystyrene (PS) has been reported to have potential toxicity toward organisms, the impact of epoxy modification on the toxicity of PS remains largely unknown. In this study, we first investigated the prolonged exposure effects of epoxy-modified PS (PS-CHO) in the range of μg/L on Caenorhabditis elegans (C. elegans) including general toxicity, target organ toxicity, and organelle toxicity. Our data revealed that C. elegans exposed to PS-CHO led to the alterations in increased lethality (≥ 1000 μg/L), shortened body length (≥ 100 μg/L), and decreased locomotion capacity (≥ 1 μg/L). In addition, toxicity analysis on target organs and organelles indicated that exposure to PS-CHO enhanced intestinal permeability (≥ 100 μg/L) by inhibiting the transcriptional levels of acs-22 (encoding fatty acid transport protein) (≥ 100 μg/L) and hmp-2 (encoding α-catenin) (≥ 1000 μg/L), reduced reproductive capacity (≥ 10 μg/L), and dysregulated mitochondrial homeostasis (≥ 1 μg/L). Moreover, the activation of antioxidant enzyme system could help nematodes against the toxicity caused by PS-CHO exposure (≥ 10 μg/L). Furthermore, we also compared the toxicity of PS-CHO with other chemically modified derivatives of PS, and the toxicity order was PS-NH > PS-SOOOH > PS-CHO > PS-COOH > PS > PS-PEG. Our study highlights the potential environmental impact of PS and its derivatives on organisms and suggests that the toxicity of nanoplastics may be charge-dependent.

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