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Polystyrene nanoplastic exposure actives ferroptosis by oxidative stress-induced lipid peroxidation in porcine oocytes during maturation
Journal of Animal Science and Biotechnology ( IF 6.3 ) Pub Date : 2024-09-03 , DOI: 10.1186/s40104-024-01077-6 Yijing He 1 , Tianhang Yu 1 , Heran Li 1, 2 , Qinfeng Sun 1 , Miaoyu Chen 1 , Yiyi Lin 1 , Jianjun Dai 2 , Weihan Wang 1 , Qiao Li 1 , Shiqiang Ju 1
Journal of Animal Science and Biotechnology ( IF 6.3 ) Pub Date : 2024-09-03 , DOI: 10.1186/s40104-024-01077-6 Yijing He 1 , Tianhang Yu 1 , Heran Li 1, 2 , Qinfeng Sun 1 , Miaoyu Chen 1 , Yiyi Lin 1 , Jianjun Dai 2 , Weihan Wang 1 , Qiao Li 1 , Shiqiang Ju 1
Affiliation
Polystyrene nanoplastics (PS-NPs) are becoming increasingly prevalent in the environment with great advancements in plastic products, and their potential health hazard to animals has received much attention. Several studies have reported the toxicity of PS-NPs to various tissues and cells; however, there is a paucity of information about whether PS-NPs exposure can have toxic effects on mammalian oocytes, especially livestock. Herein, porcine oocytes were used as the model to investigate the potential effects of PS-NPs on mammalian oocytes. The findings showed that different concentrations of PS-NPs (0, 25, 50 and 100 μg/mL) entering into porcine oocytes could induce mitochondrial stress, including a significant decrease in mitochondrial membrane potential (MMP), and the destruction of the balance of mitochondrial dynamic and micromorphology. Furthermore, there was a marked increase in reactive oxygen species (ROS), which led to oocyte lipid peroxidation (LPO). PS-NPs exposure induced abnormal intracellular iron overload, and subsequently increased the expression of transferrin receptor (TfRC), solute carrier family 7 member 11 (SLC7a11), and acyl-CoA synthetase long-chain family member 4 (ACSL4), which resulted in ferroptosis in oocytes. PS-NPs also induced oocyte maturation failure, cytoskeletal dysfunction and DNA damage. Cotreatment with 5 μmol/L ferrostatin-1 (Fer-1, an inhibitor of ferroptosis) alleviated the cellular toxicity associated with PS-NPs exposure during porcine oocyte maturation. In conclusion, PS-NPs caused ferroptosis in porcine oocytes by increasing oxidative stress and altering lipid metabolism, leading to the failure of oocyte maturation. PS-NPs could enter oocytes, caused mitochondrial dysfunction and oxidative stress, induced lipid peroxidation and ferroptosis, which eventually resulted in failure of oocyte maturation.
中文翻译:
猪卵母细胞成熟过程中,聚苯乙烯纳米塑料暴露通过氧化应激诱导的脂质过氧化激活铁死亡
随着塑料制品的巨大进步,聚苯乙烯纳米塑料(PS-NP)在环境中变得越来越普遍,其对动物健康的潜在危害受到广泛关注。多项研究报告了 PS-NP 对各种组织和细胞的毒性;然而,关于 PS-NP 暴露是否会对哺乳动物(尤其是家畜)卵母细胞产生毒性作用的信息很少。本文以猪卵母细胞为模型,研究 PS-NPs 对哺乳动物卵母细胞的潜在影响。研究结果表明,不同浓度的PS-NPs(0、25、50和100μg/mL)进入猪卵母细胞后可引起线粒体应激,包括线粒体膜电位(MMP)显着降低,线粒体平衡被破坏。线粒体动力学和微形态学。此外,活性氧(ROS)显着增加,导致卵母细胞脂质过氧化(LPO)。 PS-NPs 暴露诱导异常细胞内铁超载,随后增加转铁蛋白受体 (TfRC)、溶质载体家族 7 成员 11 (SLC7a11) 和酰基辅酶 A 合成酶长链家族成员 4 (ACSL4) 的表达,从而导致卵母细胞铁死亡。 PS-NP 还诱导卵母细胞成熟失败、细胞骨架功能障碍和 DNA 损伤。用 5 μmol/L 铁他汀-1(Fer-1,一种铁死亡抑制剂)共同处理可减轻猪卵母细胞成熟过程中与 PS-NP 暴露相关的细胞毒性。总之,PS-NPs通过增加氧化应激和改变脂质代谢而导致猪卵母细胞铁死亡,导致卵母细胞成熟失败。 PS-NPs可以进入卵母细胞,引起线粒体功能障碍和氧化应激,诱导脂质过氧化和铁死亡,最终导致卵母细胞成熟失败。
更新日期:2024-09-03
中文翻译:
猪卵母细胞成熟过程中,聚苯乙烯纳米塑料暴露通过氧化应激诱导的脂质过氧化激活铁死亡
随着塑料制品的巨大进步,聚苯乙烯纳米塑料(PS-NP)在环境中变得越来越普遍,其对动物健康的潜在危害受到广泛关注。多项研究报告了 PS-NP 对各种组织和细胞的毒性;然而,关于 PS-NP 暴露是否会对哺乳动物(尤其是家畜)卵母细胞产生毒性作用的信息很少。本文以猪卵母细胞为模型,研究 PS-NPs 对哺乳动物卵母细胞的潜在影响。研究结果表明,不同浓度的PS-NPs(0、25、50和100μg/mL)进入猪卵母细胞后可引起线粒体应激,包括线粒体膜电位(MMP)显着降低,线粒体平衡被破坏。线粒体动力学和微形态学。此外,活性氧(ROS)显着增加,导致卵母细胞脂质过氧化(LPO)。 PS-NPs 暴露诱导异常细胞内铁超载,随后增加转铁蛋白受体 (TfRC)、溶质载体家族 7 成员 11 (SLC7a11) 和酰基辅酶 A 合成酶长链家族成员 4 (ACSL4) 的表达,从而导致卵母细胞铁死亡。 PS-NP 还诱导卵母细胞成熟失败、细胞骨架功能障碍和 DNA 损伤。用 5 μmol/L 铁他汀-1(Fer-1,一种铁死亡抑制剂)共同处理可减轻猪卵母细胞成熟过程中与 PS-NP 暴露相关的细胞毒性。总之,PS-NPs通过增加氧化应激和改变脂质代谢而导致猪卵母细胞铁死亡,导致卵母细胞成熟失败。 PS-NPs可以进入卵母细胞,引起线粒体功能障碍和氧化应激,诱导脂质过氧化和铁死亡,最终导致卵母细胞成熟失败。