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聚苯乙烯微塑料通过线粒体功能障碍破坏雄性小鼠的肾上腺类固醇合成。

Polystyrene microplastics disrupt adrenal steroid synthesis in male mice via mitochondrial dysfunction.

作者信息

Xiong Ying, Chen Zhe, Xiang Hanmin, Liu Yi, Wang Yanlin

机构信息

Department of Anesthesiology, Zhongnan Hospital of Wuhan University, Wuhan University, Wuhan 430071, China.

Department of Orthopedics, Zhongnan Hospital of Wuhan University, Wuhan University, Wuhan 430071, China.

出版信息

Ecotoxicol Environ Saf. 2025 Jan 15;290:117528. doi: 10.1016/j.ecoenv.2024.117528. Epub 2024 Dec 13.

DOI:10.1016/j.ecoenv.2024.117528
PMID:39674024
Abstract

Microplastics have gained significant social attention, as they can enter our bodies through food and drinking water. The adrenal gland is essential for the maintenance of metabolic homeostasis and stress responses. Nevertheless, the effects of microplastics on the steroid synthesis in the adrenal cortex was still unclear. In this study, through both in vivo and in vitro models, we found that polystyrene microplastics (PS-MPs) impaired adrenal steroid synthesis, leading to a reduction in corticosterone levels. In vivo, we further observed that chronic exposure to PS-MPs (0.25, 0.5 and 1 mg/d for 4 weeks) could induce abnormal mitochondrial morphology and functional disruptions of adrenal glands in male mice, along with an imbalance in cellular oxidative stress, manifested as increased level of reactive oxygen species, diminished antioxidant activity (glutathione peroxidase and superoxide dismutase). In vitro, these occurrences coincided with an elevated rate of cell apoptosis observed in adrenocortical cells following exposure to PS-MPs. We proposed that mitochondrial dysfunction not only directly influenced the biosynthetic processes of steroid hormones but also induced cell apoptosis through the initiation of cellular oxidative stress. The latter may represent a common mechanism underlying the multi-organ toxicity induced by PS-MPs in the body. Our findings would provide new insights for the development of more effective environmental protection measures and the reduction of plastic pollution.

摘要

微塑料已引起社会广泛关注,因为它们可通过食物和饮用水进入人体。肾上腺对于维持代谢稳态和应激反应至关重要。然而,微塑料对肾上腺皮质类固醇合成的影响仍不清楚。在本研究中,通过体内和体外模型,我们发现聚苯乙烯微塑料(PS-MPs)损害肾上腺类固醇合成,导致皮质酮水平降低。在体内,我们进一步观察到,雄性小鼠长期暴露于PS-MPs(0.25、0.5和1毫克/天,持续4周)可诱导肾上腺线粒体形态异常和功能紊乱,同时细胞氧化应激失衡,表现为活性氧水平升高、抗氧化活性(谷胱甘肽过氧化物酶和超氧化物歧化酶)降低。在体外,这些情况与暴露于PS-MPs后的肾上腺皮质细胞凋亡率升高一致。我们认为,线粒体功能障碍不仅直接影响类固醇激素的生物合成过程,还通过引发细胞氧化应激诱导细胞凋亡。后者可能是PS-MPs在体内诱导多器官毒性的共同机制。我们的研究结果将为制定更有效的环境保护措施和减少塑料污染提供新的见解。

相似文献

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Polystyrene microplastics disrupt adrenal steroid synthesis in male mice via mitochondrial dysfunction.聚苯乙烯微塑料通过线粒体功能障碍破坏雄性小鼠的肾上腺类固醇合成。
Ecotoxicol Environ Saf. 2025 Jan 15;290:117528. doi: 10.1016/j.ecoenv.2024.117528. Epub 2024 Dec 13.
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Polystyrene microplastics exposition on human placental explants induces time-dependent cytotoxicity, oxidative stress and metabolic alterations.聚苯乙烯微塑料对人胎盘外植体的暴露会引发时间依赖性的细胞毒性、氧化应激和代谢改变。
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Polystyrene microplastics lead to pyroptosis and apoptosis of ovarian granulosa cells via NLRP3/Caspase-1 signaling pathway in rats.聚苯乙烯微塑料通过 NLRP3/Caspase-1 信号通路诱导大鼠卵巢颗粒细胞发生细胞焦亡和凋亡。
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Polystyrene micro- and nanoplastics induce gastric toxicity through ROS mediated oxidative stress and P62/Keap1/Nrf2 pathway.聚苯乙烯微塑料和纳米塑料通过 ROS 介导的氧化应激和 P62/Keap1/Nrf2 通路诱导胃毒性。
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