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In vivo assessment of bisphenol A induced histopathological alterations and inflammatory gene expression in lungs of male Wistar rats

机译:在体内评估双酚A诱导的男性Wistar大鼠肺中的组织病理学改变和炎症基因表达

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摘要

Bisphenol A (BPA), an imperative environmental contaminant used in polycarbonate plastics. Due to limited information concerning the effect of BPA on lungs, this study design to assess whether BPA cause alterations in histopathology and trace metal content in lungs of rats. They were divided into five groups with five rats per group. Group I was named as control group. Group L6 and L12 were received BPA (10 mg/kg body weight/day) for 6 weeks and 12 weeks respectively. Group H6 and L12 were given BPA (25 mg/kg body weight/day) for 6 weeks and 12 weeks respectively. Considerable alteration in Cu, Zn and Fe was detected in experimental groups. BPA also caused significant increase in the expression of tumor necrosis factor α that mediate the pulmonary inflammatory response. Comparative study of resolved proteins i.e. 72 KDa (matrix metalloproteinase 2 fragment) and 109 KDa (nucleolin) on SDS-PAGE showed their altered expression in experimental groups. Histopathology of experimental groups revealed altered architecture of lungs. Special staining of BPA treated groups showed significant number of mast cells in alveoli and bronchioles. Prolonged administration of BPA causes deleterious aggravating lung damage even at extremely low dose, so the use of BPA should be prohibited in plastic synthesizing industries.
机译:双酚A(BPA),聚碳酸酯塑料中使用的一种重要环境污染物。由于有关BPA对肺部影响的信息有限,本研究旨在评估BPA是否会引起大鼠肺部组织病理学和微量金属含量的改变。他们被分成五组,每组五只大鼠。第一组为对照组。L6组和L12组分别接受BPA(10mg/kg体重/天)治疗6周和12周。H6组和L12组分别给予BPA(25mg/kg体重/天)6周和12周。实验组中的铜、锌和铁发生了显著变化。BPA还导致介导肺部炎症反应的肿瘤坏死因子α表达显著增加。在SDS-PAGE上对分离蛋白72 KDa(基质金属蛋白酶2片段)和109 KDa(核仁蛋白)的比较研究表明,它们在实验组中的表达发生了改变。实验组的组织病理学显示肺结构改变。BPA处理组的特殊染色显示肺泡和细支气管中有大量肥大细胞。即使在极低剂量下,长期服用双酚A也会导致有害的加重肺损伤,因此应禁止在塑料合成行业使用双酚A。

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