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Sci Total Environ ; 913: 169730, 2024 Feb 25.
Article in English | MEDLINE | ID: mdl-38160834

ABSTRACT

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 via 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 in vivo and in vitro 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 N-acetyl-L-cysteine and pifithrin-α for in vitro intervention and found that N-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.


Subject(s)
Benzhydryl Compounds , Benzothiazoles , Phenols , Selenium , Toluene/analogs & derivatives , Animals , Reactive Oxygen Species/metabolism , Selenium/toxicity , Selenium/metabolism , Chickens/metabolism , Tumor Suppressor Protein p53/metabolism , Acetylcysteine/pharmacology , Molecular Docking Simulation , Oxidative Stress , Intestines , Apoptosis , Cell Cycle Checkpoints
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