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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. Detection Methods Human Health Effects Nanoplastics Remediation Sign in to save

Metabolomics Reveal Nanoplastic-Induced Mitochondrial Damage in Human Liver and Lung Cells

Environmental Science & Technology 2022 333 citations ? Citation count from OpenAlex, updated daily. May differ slightly from the publisher's own count. Score: 65 ? 0–100 AI score estimating relevance to the microplastics field. Papers below 30 are filtered from public browse.
Pengfei Wu, Pengfei Wu, Pengfei Wu, Pengfei Wu, Pengfei Wu, Pengfei Wu, Pengfei Wu, Zongwei Cai, Ming Hung Wong Pengfei Wu, Pengfei Wu, Pengfei Wu, Pengfei Wu, Chen Wang, Siyi Lin, Pengfei Wu, Zongwei Cai, Zongwei Cai, Zongwei Cai, Pengfei Wu, Zhu Yang, Pengfei Wu, Hongna Zhang, Hongna Zhang, Siyi Lin, Siyi Lin, Chen Wang, Zhu Yang, Zongwei Cai, Chunmiao Zheng, Ming Hung Wong Ming Hung Wong Chunmiao Zheng, Xiuli Su, Pengfei Wu, Zongwei Cai, Pengfei Wu, Zongwei Cai, Siyi Lin, Chen Wang, Xiuli Su, Yuanyuan Song, Ming Hung Wong Pengfei Wu, Chen Wang, Zongwei Cai, Yuanyuan Song, Chen Wang, Chen Wang, Zongwei Cai, Zhu Yang, Zongwei Cai, Zongwei Cai, Zongwei Cai, Zongwei Cai, Zongwei Cai, Zongwei Cai, Zongwei Cai, Zongwei Cai, Zongwei Cai, Pengfei Wu, Zongwei Cai, Chen Wang, Zongwei Cai, Pengfei Wu, Pengfei Wu, Ming Hung Wong Pengfei Wu, Zhu Yang, Ming Hung Wong Zhu Yang, Ming Hung Wong Zongwei Cai, Ming Hung Wong Pengfei Wu, Zhu Yang, Zongwei Cai, Chunmiao Zheng, Chunmiao Zheng, Chunmiao Zheng, Zongwei Cai, Ming Hung Wong Zongwei Cai, Ming Hung Wong Chunmiao Zheng, Zhu Yang, Zongwei Cai, Zongwei Cai, Ming Hung Wong Zongwei Cai, Zhu Yang, Zongwei Cai, Zongwei Cai, Zongwei Cai, Ming Hung Wong Zongwei Cai, Chunmiao Zheng, Zongwei Cai, Zongwei Cai, Ming Hung Wong

Summary

Researchers exposed normal human liver and lung cells to 80-nanometer plastic particles and found that the nanoplastics damaged mitochondria, the energy-producing structures inside cells, without causing widespread cell death. Using metabolomics analysis, they identified specific disruptions to energy metabolism and lipid processing pathways in both cell types. This study reveals a subtle but important way that nanoplastics could impair organ function in humans by disrupting cellular energy production.

Plastic debris in the global biosphere is an increasing concern, and nanoplastic (NPs) toxicity in humans is far from being understood. Studies have indicated that NPs can affect mitochondria, but the underlying mechanisms remain unclear. The liver and lungs have important metabolic functions and are vulnerable to NP exposure. In this study, we investigated the effects of 80 nm NPs on mitochondrial functions and metabolic pathways in normal human hepatic (L02) cells and lung (BEAS-2B) cells. NP exposure did not induce mass cell death; however, transmission electron microscopy analysis showed that the NPs could enter the cells and cause mitochondrial damage, as evidenced by overproduction of mitochondrial reactive oxygen species, alterations in the mitochondrial membrane potential, and suppression of mitochondrial respiration. These alterations were observed at NP concentrations as low as 0.0125 mg/mL, which might be comparable to the environmental levels. Nontarget metabolomics confirmed that the most significantly impacted processes were mitochondrial-related. The metabolic function of L02 cells was more vulnerable to NP exposure than that of BEAS-2B cells, especially at low NP concentrations. This study identifies NP-induced mitochondrial dysfunction and metabolic toxicity pathways in target human cells, providing insight into the possibility of adverse outcomes in human health.

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