...
  • 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>The Journal of toxicological sciences >Induction of apoptosis and CYP4A1 expression in Sprague-Dawley rats exposed to low doses of perfluorooctane sulfonate
【24h】

Induction of apoptosis and CYP4A1 expression in Sprague-Dawley rats exposed to low doses of perfluorooctane sulfonate

机译：低剂量全氟辛烷磺酸暴露的Sprague-Dawley大鼠的细胞凋亡和CYP4A1表达的诱导

获取原文
           
页面导航
  • 摘要
  • 著录项
  • 相似文献
  • 相关主题

摘要

In previous studies, perfluorooctane sulfonate (PFOS), an environmental organic compound, was reported to cause hepatotoxicity and hypolipidemia in rodents. However, the low dose toxicity of PFOS and the toxic mechanisms involved remain to be determined. To clarify the low dose toxicity and action mechanism in the target organ toxicity, Sprague-Dawley (SD) rats were orally administered with PFOS at the doses of 0, 1.25, 5, 10 mg/kg/day for 28 days. As a result, no death or abnormal symptoms were observed in all groups. The significant loss of mean body weight was observed in female rats treated with 10 mg/kg PFOS and the relative liver weight of 10 mg/kg PFOS-treated group was significantly greater compared to control. Histopathological examination revealed that fatty change was evident in the liver of male rats treated with PFOS (5 and 10 mg/kg) and hypertrophy and cellular swellings in females at the dose of 10 mg/kg, which showed different pattern of pathological lesions. In addition, we demonstrated the expression induction of hepatic caspase-3 and cytochrome P450 4A1 (CYP4A1) related with apoptosis and lipid metabolism, respectively. This study suggested that no-observed-adverse-effect level (NOAEL) of PFOS was 1.25 mg/kg in 28-day repeated toxicity study and, however, the toxic response showed gender differences. The possible toxic mechanism of PFOS was the induction of apoptosis and altering lipid metabolism which resulted in hepatotoxicity.
机译：在先前的研究中，据报道，全氟辛烷磺酸盐（PFOS）是一种环境有机化合物，可引起啮齿动物的肝毒性和低血脂症。但是，全氟辛烷磺酸的低剂量毒性及其所涉及的毒性机制仍有待确定。为了阐明低剂量毒性和靶器官毒性的作用机理，对Sprague-Dawley（SD）大鼠口服全氟辛烷磺酸，剂量为0、1.25、5、10 mg / kg / day，共28天。结果，在所有组中均未观察到死亡或异常症状。在用10 mg / kg PFOS治疗的雌性大鼠中观察到平均体重的显着下降，与对照组相比，用10 mg / kg PFOS治疗的组的相对肝脏重量明显更大。组织病理学检查显示，在用全氟辛烷磺酸（5和10 mg / kg）处理的雄性大鼠的肝脏中，脂肪变化明显，而在雌性大鼠中，以10 mg / kg的剂量，肥大和细胞肿胀明显，这显示出不同的病理病变模式。此外，我们证明了肝胱天蛋白酶-3和细胞色素P450 4A1（CYP4A1）的表达诱导分别与细胞凋亡和脂质代谢有关。这项研究表明，在28天的重复毒性研究中，未观察到的全氟辛烷磺酸不良反应水平（NOAEL）为1.25 mg / kg，但是毒性反应显示出性别差异。全氟辛烷磺酸可能的毒性机制是诱导细胞凋亡和改变脂质代谢，从而导致肝毒性。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
获取原文

客服邮箱：kefu@zhangqiaokeyan.com

京公网安备：11010802029741号 ICP备案号：京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有

  • 客服微信

  • 服务号