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在体外实验中,微塑料通过引发与骨骼肌中活性氧相关的线粒体功能障碍来诱导胰岛素抵抗。

Microplastics induce insulin resistance by causing mitochondrial dysfunction associated with mROS in skeletal muscle in vitro.

作者信息

Tang Yuzhen, Suo Yaxin, Sun Zewen, Wu Xiafang, Xing Qingyang, Bai Yinglong

机构信息

Department of Maternal and Child Health, School of Public Health, China Medical University, Shenyang, China.

Department of Maternal and Child Health, School of Public Health, China Medical University, Shenyang, China; Shandong Cancer Hospital and Institute, Shandong First Medical University and Shandong Academy of Medical Sciences, Jinan, China.

出版信息

Ecotoxicol Environ Saf. 2025 Sep 1;302:118585. doi: 10.1016/j.ecoenv.2025.118585. Epub 2025 Jun 30.

DOI:10.1016/j.ecoenv.2025.118585
PMID:40592146
Abstract

Microplastics pose an emerging threat to both ecological and human health. It is worth noting that muscle has proved to be the target organ of microplastic particles. Skeletal muscle is the major site of insulin-stimulated glucose disposal and subsequent glucose homeostasis and plays a key role in the regulation of glucose metabolism in the body. However, studies on the effects of microplastics on glucose metabolism and insulin sensitivity in human skeletal muscle are limited. Herein, human rhabdomyosarcoma (RD) cells were exposed to two sizes (3 μm and 100 nm) of polystyrene microplastics/nanoplastics (PS-MPs/NPs) at three concentrations (75, 150, and 300 μg/mL) to investigate the possible molecular mechanisms. Our results showed that PS-MPs/NPs could be internalized into RD cells and lead to a reduction in cellular uptake of glucose. These results suggest that PS-MPs/NPs may cause skeletal muscle insulin resistance (IR) at the cellular level. Additionally, we observed that PS-MPs/NPs not only resulted in mitochondrial damage but also induced intracellular oxidative stress. However, treatment with the mitochondria-targeted antioxidant MitoQ improved mitochondrial dysfunction and IR at the cellular level. These findings indicate that PS-MPs/NPs induce IR by causing mitochondrial dysfunction associated with mROS in skeletal muscle in vitro. The identification of these molecular mechanisms is helpful for deeply understanding of the health hazards posed by microplastics.

摘要

微塑料对生态和人类健康构成了新出现的威胁。值得注意的是,肌肉已被证明是微塑料颗粒的靶器官。骨骼肌是胰岛素刺激的葡萄糖处置及随后的葡萄糖稳态的主要部位,在调节体内葡萄糖代谢中起关键作用。然而,关于微塑料对人体骨骼肌葡萄糖代谢和胰岛素敏感性影响的研究有限。在此,将人横纹肌肉瘤(RD)细胞暴露于三种浓度(75、150和300μg/mL)的两种尺寸(3μm和100nm)的聚苯乙烯微塑料/纳米塑料(PS-MPs/NPs)中,以研究可能的分子机制。我们的结果表明,PS-MPs/NPs可被内化到RD细胞中,并导致细胞对葡萄糖的摄取减少。这些结果表明,PS-MPs/NPs可能在细胞水平上导致骨骼肌胰岛素抵抗(IR)。此外,我们观察到PS-MPs/NPs不仅导致线粒体损伤,还诱导细胞内氧化应激。然而,用线粒体靶向抗氧化剂MitoQ处理可改善细胞水平的线粒体功能障碍和IR。这些发现表明,PS-MPs/NPs在体外通过引起与骨骼肌中mROS相关的线粒体功能障碍来诱导IR。这些分子机制的确定有助于深入了解微塑料所造成的健康危害。

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引用本文的文献

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Mitochondrial Dysfunction and Oxidative Stress: Emerging Insights in Muscle and Cardiovascular Disease Mechanisms.线粒体功能障碍与氧化应激:肌肉和心血管疾病机制的新见解
Antioxidants (Basel). 2025 Jul 23;14(8):902. doi: 10.3390/antiox14080902.