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Synergistic effects of nanoplastics and BDE-47 on glutathione dysregulation in rice: Insights from integrated multi-omics and computational modeling
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Scientists found that tiny plastic particles and a common flame retardant chemical (BDE-47, found in older furniture and electronics) become more toxic together than either one alone when they affect rice plants, messing with the plant's natural defense system and stunting its growth. This matters because rice is a staple food for billions of people, and if nanoplastics and chemical pollutants team up to harm crops in the field the same way they did in this study, it could mean lower harvests and raises questions about what ends up on our plates. While this research was done in plants, not humans, it's an early warning sign that these two increasingly common pollutants may interact in ways that are
Understanding the combined toxicity mechanisms of polybrominated diphenyl ethers (PBDEs) and nanoplastics is essential for ecological risk management. This study integrated physiological, transcriptomic, metabolomic, and computational analyses to investigate the synergistic phytotoxicity of polyethylene (PE) nanoplastics and 2,2',4,4'-Tetrabromodiphenyl ether (BDE-47) in rice (Oryza sativa L.). Co-exposure synergistically intensified toxicity compared to isolated treatments, causing 14.8 %-42.8 % reductions (P < 0.001) in enzymatic antioxidants such as peroxidase (POD), catalase (CAT), superoxide dismutase (SOD), ascorbate peroxidase (APX) activities and non-enzymatic antioxidants oxidized glutathione (GSSG) and ascorbate (AsA) levels, alongside inhibited root and shoot growth. Transcriptomic data revealed suppressed expression of photosystem II genes (psbO, psbW), correlating with impaired photosynthesis, energy deficits, and growth restriction. Concurrently, glutathione biosynthesis genes (OsGLN2, OsGS1, OsGPX1/4) were downregulated, disrupting glutamine-to-glutathione (GSH) conversion. Metabolomic analysis confirmed 3.5-fold glutamate depletion and inhibited carbohydrate metabolism, indicating pollutant-induced oxidative stress. Molecular docking simulations identified OsGPX1 as BDE-47's binding target through hydrogen-bond interactions, which competitively blocked GSH binding to glutathione peroxidase (GPX). This demonstrated that nanoplastics act as chemical potentiators, amplifying PBDEs toxicity via enzyme inhibition and metabolic interference. Specifically, PE enhanced BDE-47's capacity to disrupt redox homeostasis and energy metabolism through direct protein interactions and pathway dysregulation. These findings would provide mechanistic insights into pollutant synergism, emphasizing the need to evaluate nanoplastic co-contaminants in environmental risk frameworks.
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