在猪卵母细胞成熟过程中,通过氧化应激诱导的脂质过氧化反应,聚苯乙烯纳米塑料暴露可激活铁突变。

IF 6.3 Q1 AGRICULTURE, DAIRY & ANIMAL SCIENCE
Yijing He, Tianhang Yu, Heran Li, Qinfeng Sun, Miaoyu Chen, Yiyi Lin, Jianjun Dai, Weihan Wang, Qiao Li, Shiqiang Ju
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引用次数: 0

摘要

背景:随着塑料产品的巨大进步,聚苯乙烯纳米塑料(PS-NPs)在环境中越来越普遍,其对动物健康的潜在危害也受到了广泛关注。已有多项研究报道了 PS-NPs 对不同组织和细胞的毒性,但有关 PS-NPs 暴露是否会对哺乳动物卵母细胞(尤其是家畜)产生毒性影响的信息却很少。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:结果:研究结果表明,不同浓度的 PS-NPs (0、25、50 和 100 μg/mL)进入猪卵母细胞可诱导线粒体应激,包括线粒体膜电位(MMP)显著降低、线粒体动态平衡和微形态破坏。此外,活性氧(ROS)明显增加,导致卵母细胞脂质过氧化(LPO)。暴露于 PS-NPs 会诱导细胞内铁异常超载,进而增加转铁蛋白受体(TfRC)、溶质运载体家族 7 成员 11(SLC7a11)和酰基-CoA 合成酶长链家族成员 4(ACSL4)的表达,导致卵母细胞铁突变。PS-NPs 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 铁前列素-1(Fer-1,一种铁突变抑制剂)共处理可减轻猪卵母细胞成熟过程中与 PS-NPs 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引起猪卵母细胞铁变态反应,导致卵母细胞成熟失败。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Polystyrene nanoplastic exposure actives ferroptosis by oxidative stress-induced lipid peroxidation in porcine oocytes during maturation.

Background: 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.

Results: 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.

Conclusions: In conclusion, PS-NPs caused ferroptosis in porcine oocytes by increasing oxidative stress and altering lipid metabolism, leading to the failure of oocyte maturation.

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CiteScore
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