刘小燕,屈 艾,胡方方,杨亚茹,曹义娟.全氟辛烷磺酸钾对小鼠肾脏的氧化性损伤[J].现代生物医学进展英文版,2017,17(20):3842-3845. |
全氟辛烷磺酸钾对小鼠肾脏的氧化性损伤 |
Oxidative Damage on Kidney of Mice Induced by PFOS-K |
Received:November 08, 2016 Revised:November 29, 2016 |
DOI:10.13241/j.cnki.pmb.2017.20.009 |
中文关键词: 全氟辛烷磺酸钾 小鼠 肾脏脏器系数 肾脏氧化损伤 生化毒性 |
英文关键词: PFOS-K Mice Kidney organ coefficient Oxidative damage Biochemical toxicity |
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中文摘要: |
摘要 目的:以小鼠肾脏细胞中的活性氧(ROS)、丙二醛(MDA)、谷胱甘肽(GSH)含量和超氧化物歧化酶(SOD)、谷胱甘肽过氧化物酶(GSH-Px)、过氧化氢酶(CAT)活力为指标,探讨全氟辛烷磺酸钾(PFOS-K)对小鼠肾脏的氧化性损伤作用。方法:以剂量为6 mg/kg?bw、12 mg/kg?bw、24 mg/kg?bw 3个浓度的PFOS-K混悬液,每天分别给小鼠经口灌胃一次,连续染毒20天后检测肾脏脏器系数,以及肾脏中ROS、MDA、GSH含量的变化和SOD、GSH-Px、CAT活性的改变。结果:与阴性对照组相比,在6-24 mg/kg?bw剂量范围内,PFOS-K使小鼠体重下降、肾脏重量增加、肾脏脏器系数增大,且表现出一定的剂量-效应关系(r小鼠体重=-0.905, r肾脏湿重=0.938, r脏器系数=0.936)。PFOS-K使小鼠肾脏内活性氧(ROS)及丙二醛(MDA)含量增多(rROS=0.990, rMDA=0.997)、谷胱甘肽(GSH)含量减少(rGSH= -0.994),超氧化物歧化酶(SOD)、谷胱甘肽过氧化物酶(GSH-Px)、过氧化氢酶(CAT)活力降低(rSOD= -0.917, rGSH-Px= -0.986, rCAT=-0.991)。结论:本试验条件下,PFOS-K致使小鼠肾脏肿大,影响了肾脏的发育;造成了肾脏的氧化性损伤,肾组织内抗氧化酶系统遭到破坏,氧化应激反应增强,具有氧化损伤作用。 |
英文摘要: |
ABSTRACT Objective: To investigate oxidative damage on the kidney of mice induced by PFOS-K with ROS, MDA, GSH, SOD, GSH PX and CAT as indicators. Methods: The mice were gavaged with three doses of PFOS-K (6, 12, 24 mg/kg.bw). The organ coefficient of kidney was measured and ROS, MDA, GSH contents were detected and the activities of SOD, GSH-Px, CAT after 20 days. Results: With the increasing dose of PFOS-K, the body weight decreased, the kidney weight and the renal organ coefficient increased in mice. And it showed a dose-response relationship (rbody weight= -0.905, rkidney wet weight=0.938, rorgan coefficient=0.936). And in 6 to 24 mg/kg.bw dose PFOS-K group, the contents of ROS, MDA were increased(rROS=0.990, rMDA=0.997), the GSH was decreased(rGSH= -0.994), and the SOD, GSH-Px and CAT activity were dropped(rSOD=-0.917, rGSH-Px= -0.986, rCAT= -0.991). Conclusion: The results indicated that, PFOS-K caused the mice kidney enlargement, affected the development of the kidney, caused the oxidative damage of the kidneys, destructed the antioxidant enzyme system and enhanced oxidative stress. |
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