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Selenium deficiency exacerbated Bisphenol A-induced intestinal toxicity in chickens: Apoptosis and cell cycle arrest mediated by ROS/P53
Science of the Total Environment ( IF 8.2 ) Pub Date : 2023-12-30 , DOI: 10.1016/j.scitotenv.2023.169730 Dongliu Luo 1 , Xinyu Tang 1 , Yixuan Wang 1 , Shuqi Ying 1 , Yujiao He 2 , Hongjin Lin 1 , Pervez Ahmed Khoso 3 , Shu Li 1
Science of the Total Environment ( IF 8.2 ) Pub Date : 2023-12-30 , DOI: 10.1016/j.scitotenv.2023.169730 Dongliu Luo 1 , Xinyu Tang 1 , Yixuan Wang 1 , Shuqi Ying 1 , Yujiao He 2 , Hongjin Lin 1 , Pervez Ahmed Khoso 3 , Shu Li 1
Affiliation
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Bisphenol A (BPA) is a phenolic organic synthetic compound that is used as the raw material of polycarbonate plastics, and its safety issues have recently attracted wide attention. Selenium (Se) deficiency has gradually developed into a global disease affecting intestinal function oxidative stress and apoptosis. However, the toxic effects and potential mechanisms of BPA exposure and Se deficiency in the chicken intestines have not been studied. In this study, BPA exposure and/or Se deficiency models were established and to investigate the effects of Se deficiency and BPA on chicken jejunum. The results showed that BPA exposure and/or Se deficiency increased jejunum oxidative stress and DNA damage, activated P53 pathway, led to mitochondrial dysfunction, and induced apoptosis and cell cycle arrest. Using protein-protein molecular docking, we found a strong binding ability between P53 and peroxisome proliferator-activated receptor γ coactivator-1, thereby regulating mitochondrial dysfunctional apoptosis. In addition, we used -acetyl-L-cysteine and pifithrin-α for intervention and found that -acetyl-L-cysteine and pifithrin-α intervention reversed the aforementioned adverse effects. This study clarified the potential mechanism by which Se deficiency exacerbates BPA induced intestinal injury in chickens through reactive oxygen species/P53, which provides a new idea for the study of environmental combined toxicity of Se deficiency, and insights into animal intestinal health from a new perspective.
中文翻译：
缺硒加剧了双酚 A 诱导的鸡肠道毒性：ROS/P53 介导的细胞凋亡和细胞周期停滞
双酚A（BPA）是一种酚类有机合成化合物，用作聚碳酸酯塑料的原料，其安全问题近年来引起广泛关注。硒（Se）缺乏已逐渐发展成为影响肠道功能氧化应激和细胞凋亡的全球性疾病。然而，双酚 A 暴露和缺硒对鸡肠道的毒性作用和潜在机制尚未研究。本研究建立了BPA暴露和/或硒缺乏模型，并研究硒缺乏和BPA对鸡空肠的影响。结果表明，BPA暴露和/或硒缺乏会增加空肠氧化应激和DNA损伤，激活P53通路，导致线粒体功能障碍，并诱导细胞凋亡和细胞周期停滞。通过蛋白质-蛋白质分子对接，我们发现P53与过氧化物酶体增殖物激活受体γ辅激活物-1之间具有很强的结合能力，从而调节线粒体功能失调的细胞凋亡。此外，我们使用-乙酰-L-半胱氨酸和pifithrin-α进行干预，发现-乙酰-L-半胱氨酸和pifithrin-α干预逆转了上述不良反应。该研究阐明了缺硒通过活性氧/P53加剧BPA引起鸡肠道损伤的潜在机制，为缺硒环境复合毒性研究提供了新思路，从新角度洞察动物肠道健康。
更新日期：2023-12-30
中文翻译：
缺硒加剧了双酚 A 诱导的鸡肠道毒性：ROS/P53 介导的细胞凋亡和细胞周期停滞
双酚A（BPA）是一种酚类有机合成化合物，用作聚碳酸酯塑料的原料，其安全问题近年来引起广泛关注。硒（Se）缺乏已逐渐发展成为影响肠道功能氧化应激和细胞凋亡的全球性疾病。然而，双酚 A 暴露和缺硒对鸡肠道的毒性作用和潜在机制尚未研究。本研究建立了BPA暴露和/或硒缺乏模型，并研究硒缺乏和BPA对鸡空肠的影响。结果表明，BPA暴露和/或硒缺乏会增加空肠氧化应激和DNA损伤，激活P53通路，导致线粒体功能障碍，并诱导细胞凋亡和细胞周期停滞。通过蛋白质-蛋白质分子对接，我们发现P53与过氧化物酶体增殖物激活受体γ辅激活物-1之间具有很强的结合能力，从而调节线粒体功能失调的细胞凋亡。此外，我们使用-乙酰-L-半胱氨酸和pifithrin-α进行干预，发现-乙酰-L-半胱氨酸和pifithrin-α干预逆转了上述不良反应。该研究阐明了缺硒通过活性氧/P53加剧BPA引起鸡肠道损伤的潜在机制，为缺硒环境复合毒性研究提供了新思路，从新角度洞察动物肠道健康。
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