Charaya Aarzoo, Sahu Chittaranjan, Singla Shivani, Jena Gopabandhu
Facility for Risk Assessment and Intervention Studies, Department of Pharmacology and Toxicology, National Institute of Pharmaceutical Education and Research, S.A.S Nagar, Sahibzada Ajit Singh Nagar, Punjab, India, 160062.
Biol Trace Elem Res. 2023 Jun;201(6):2879-2894. doi: 10.1007/s12011-022-03392-3. Epub 2022 Sep 8.
Zinc (Zn) plays an important role in the maintenance of redox status in the biological system. Zn deficiency has been found to be associated with negative effects on the functioning of many organ systems, including hepatic and renal systems. Bisphenol A (BPA) can alter Zn homeostasis and perturb the physiological system by provoking oxidative stress, which can lead to damage of different organs such as reproductive, immune, neuroendocrine, hepatic and renal systems. The present study aims to investigate the toxicity of BPA in Zn deficient condition in the liver and kidney of rat and to correlate its synergistic actions. Zn deficiency was induced by feeding Zn-deficient diet (ZDD), and BPA was administered orally (100 mg/kg/d). Male Sprague-Dawley rats were divided into four groups: NPD + Vehicle (normal feed and water), NPD + BPA (100 mg/kg/d), ZDD + Vehicle (fed with Zn-deficient diet only) and ZDD + BPA (Zn-deficient diet + BPA; 100 mg/kg/d) for 8 weeks. Biochemical, histopathological, TUNEL assay and protein expression profiles were determined to decipher the oxidative damage induced by ZDD and the toxicant BPA. Expression profile of nuclear factor erythroid 2-related factor 2, proliferating cell nuclear antigen, kelch-like ECH-associated protein 1, superoxide dismutase-1, metallothionein and apoptosis incidence showed that ZDD and BPA have a synergistic exacerbation effect on the liver and kidney of rat.
锌（Zn）在维持生物系统的氧化还原状态中起着重要作用。已发现锌缺乏与包括肝脏和肾脏系统在内的许多器官系统功能的负面影响有关。双酚A（BPA）可通过引发氧化应激改变锌稳态并扰乱生理系统，这可能导致生殖、免疫、神经内分泌、肝脏和肾脏等不同器官的损伤。本研究旨在探讨双酚A在大鼠肝脏和肾脏锌缺乏条件下的毒性，并关联其协同作用。通过喂食缺锌饮食（ZDD）诱导锌缺乏，口服给予双酚A（100mg/kg/d）。将雄性Sprague-Dawley大鼠分为四组：正常饲料+溶剂（正常饲料和水）、正常饲料+BPA（100mg/kg/d）、缺锌饲料+溶剂（仅喂食缺锌饮食）和缺锌饲料+BPA（缺锌饮食+BPA；100mg/kg/d），持续8周。测定生化、组织病理学、TUNEL检测和蛋白质表达谱，以解读缺锌饮食和有毒物质双酚A诱导的氧化损伤。核因子红细胞2相关因子2、增殖细胞核抗原、kelch样ECH相关蛋白1、超氧化物歧化酶-1、金属硫蛋白的表达谱和细胞凋亡发生率表明，缺锌饮食和双酚A对大鼠肝脏和肾脏具有协同加剧作用。
