锰对大鼠肝脏线粒体氧化损伤的作用机制

申玲; 贾克

留言板

尊敬的读者、作者、审稿人, 关于本刊的投稿、审稿、编辑和出版的任何问题, 您可以本页添加留言。我们将尽快给您答复。谢谢您的支持!

姓名
邮箱
手机号码
标题
留言内容
验证码

锰对大鼠肝脏线粒体氧化损伤的作用机制

申玲 , 贾克

文章导航 > 蚌埠医学院学报 > 2011, 36 > 12: (1293-1295)

引用本文:

Citation:

锰对大鼠肝脏线粒体氧化损伤的作用机制

申玲,
贾克^,

蚌埠医学院预防医学系, 安徽蚌埠 233030

作者简介: 申玲(1973-),女,实验师.

通讯作者: 贾克, 讲师.jake981005@126.com

基金项目:
蚌埠医学院自然科学研究资助项目(BY0834)
中图分类号: R595.2

The mechanism of manganese induced oxidative damage on rat liver mitochondria

SHEN Ling,
JIA Ke^,

Department of Preventive Medicine, Bengbu Medical College, Bengbu Anhui 233030, China

Corresponding author: JIA Ke, 讲师.jake981005@126.com

CLC number: R595.2

摘要: 目的:观察不同剂量的锰对大鼠肝脏线粒体的氧化损伤作用,探讨其相关机制。方法:将24只雄性SD大鼠随机均分为对照组和MnCl₂低、中、高剂量组,分别腹腔注射生理盐水和2、8、32 g/kg MnCl₂溶液,每天1次,连续30 d后取大鼠肝组织测定线粒体PT孔、线粒体膜肿胀度、线粒体膜电位、琥珀酸脱氢酶(SDH)、细胞色素C、羟自由基(OH·)和谷胱甘肽过氧化物酶(GSH-PX)。结果:各组间肝线粒体PT孔差异均有统计学意义(P<0.01);MnCl₂高剂量组线粒体膜肿胀度小于对照组和MnCl₂低剂量组(P<0.05);MnCl₂高剂量组线粒体膜电位光密度均低于其他3组(P<0.05~P<0.01)。与对照组和MnCl₂低剂量组相比,MnCl₂中、高剂量组肝线粒体SDH均下降(P<0.01),且MnCl₂中、高剂量组间差异亦有统计学意义(P<;与对照组和MnCl₂低剂量组相比,MnCl₂高剂量组肝线粒体细胞色素C上升(P<0.05)。MnCl₂高剂量组肝线粒体OH·显著高于其他3组(P<0.01);与对照组比较,MnCl₂低、中、高剂量组大鼠肝线粒体GSH-PX显著降低(P<0.05)。结论:锰可导致线粒体氧化损伤,引起大鼠肝线粒体PT孔开放、膜电位下降,SDH、GSH-PX降低,细胞色素C、OH·显著升高,对机体产生毒性作用。
- 锰 /
- 肝脏线粒体 /
- 氧化损伤 /
- 大鼠
Abstract: Objective:To observe the oxidative damage of rat liver mitochondria induced by different doses of manganese and explore the related mechanism. Methods:Twenty four male SD rats were divided into 4 groups,6 rats in each group,including control group,low dose group,medium dose group and high dose group. The rats in control group were injected normal saline intraperitoneally and the rats in low dose, medium and high dose groups were injected 2 g·kg^-1·d^-1, 8 g·kg^-1·d^-1 and 32 g·kg^-1·d^-1 MnCl₂ intraperitoneally respectively for 30 days. The rat liver tissue was extracted and mitochondria suspension was obtained by differential centrifugation separation to measure mitochondrial PT pore,the degree of mitochondrial swelling,the mitochondrial membrane potential and the content of succinate dehydrogenase (SDH), cytochrome C, hydroxyl radical OH·and glutathione peroxidase (GSH-PX). Results:The mitochondrial PT pore in the four groups was different and the differences had statistical significances(P<0.01); the mitochondrial swelling degree in high dose group was lower than that in control and low dose group(P<0.05); the mitochondrial membrane potential in high dose group was decreased compared with that of other groups(P<0.05-P<0.01); the content of SDH in medium and high dose group was decreased compared with that in control and low dose group(P<0.01) and the difference of SDH between medium and high dose group had statistical significance(P<0.01); the cytochrome C content in high dose group was higher than that in control and low dose group(P<0.05); the content of hydroxyl radical OH·in high dose group was increased compared with that in other three groups (P<0.01); in the same time, the content of GSH-PX in low, medium and high groups decreased compared with that in control group(P<0.05). Conclusions:Manganese can induce mitochondrial oxidative damage. Manganese has the toxic effects on rat mitochondria and the toxic effects induce rat liver mitochondrial PT pore opening,decreasing the optical density of membrane potential and the content of SDH and GSH-PX,increasing the content of cytochrome C and hydroxyl radical OH·significantly.
- manganese /
- liver mitochondria /
- oxidative damage /
- rats

[1]	王建军 , 贾克 . 牛磺酸和环孢素A对氯化锰致大鼠肝脏线粒体氧化损伤作用的影响. 蚌埠医学院学报, 2010, 35(12): 1217-1219.
[2]	贾克 , 张立丰 . 氯化锰对大鼠纹状体和大脑皮质谷氨酸含量的影响. 蚌埠医学院学报, 2008, 33(4): 389-391.
[3]	张朋 , 陈冲 , 张凡 , 杜首楠 , 周礼华 . 氯氰菊酯对雄性小鼠肝脏组织的氧化损伤. 蚌埠医学院学报, 2015, 40(11): 1479-1481. doi: 10.13898/j.cnki.issn.1000-2200.2015.11.006
[4]	方迎艳 , 马丽 , 关宿东 . 绞股蓝总皂甙对阿霉素致大鼠膈肌收缩功能及线粒体超微结构损伤的影响. 蚌埠医学院学报, 2010, 35(2): 117-120.
[5]	王栓虎 , 姜从桥 . 硫普罗宁和脾切除对大鼠肝脏缺血再灌注损伤的保护作用. 蚌埠医学院学报, 2009, 34(11): 962-965.
[6]	方典 , 梁欢 , 王佳慧 , 汪敬业 , 李正红 , 高琴 . 线粒体细胞色素c释放抑制剂对大鼠全脑缺血再灌注损伤炎症反应的作用. 蚌埠医学院学报, 2022, 47(1): 7-12. doi: 10.13898/j.cnki.issn.1000-2200.2022.01.002
[7]	徐丙发 , 吴华璞 , 祝晓光 . 姜黄素对大鼠缺血再灌注损伤的保护作用. 蚌埠医学院学报, 2007, 32(6): 637-639,765.
[8]	王力 , 张梦媛 , 吕卉 , 申玲 , 张玉媛 , 赵文红 . 全氟辛酸致小鼠脾脏氧化损伤的实验研究. 蚌埠医学院学报, 2015, 40(6): 716-718. doi: 10.13898/j.cnki.issn.1000-2200.2015.06.005
[9]	黄丽 , 王春 , 赵士弟 . 针刺预处理对大鼠小脑浦肯野细胞缺血性损伤的影响. 蚌埠医学院学报, 2016, 41(1): 7-9,15. doi: 10.13898/j.cnki.issn.1000-2200.2016.01.002
[10]	周燕妮 , 章宏 , 张玉媛 . Nrf2在镉诱导的氧化损伤和致癌中保护作用的研究进展. 蚌埠医学院学报, 2017, 42(8): 1149-1151. doi: 10.13898/j.cnki.issn.1000-2200.2017.08.045
[11]	周礼华 , 陈冲 , 张朋 , 王力 , 吴学森 . 氯氰菊酯对小鼠小脑组织氧化损伤及核转录因子-E2相关因子2基因表达的影响. 蚌埠医学院学报, 2016, 41(7): 845-848,853. doi: 10.13898/j.cnki.issn.1000-2200.2016.07.002
[12]	侯晞 , 梁枫 , 李爱剑 , 王灿 , 戴体俊 , 桂常青 . 银杏叶提取物联合依达拉奉对气虚血瘀型脑缺血再灌注损伤大鼠脑组织NO及NOS表达的影响. 蚌埠医学院学报, 2011, 36(7): 673-676.
[13]	高金霞 , 常旭红 , 张玉媛 , 王允 , 王春华 , 申玲 . 三氯乙烯致大鼠肾脏氧化损伤的实验研究. 蚌埠医学院学报, 2012, 36(12): 1405-1406.
[14]	郭宏焘 , 阮彩莲 . 慢性间歇低氧训练对大鼠心肌线粒体ATP酶的影响. 蚌埠医学院学报, 2015, 40(10): 1315-1317.
[15]	代应辉 , 李寿玲 , 朱美玲 , 陈逖 . 大鼠高眼压视网膜缺血再灌注损伤形态学改变. 蚌埠医学院学报, 2005, 30(5): 385-387.
[16]	赵瑾 , 杨卫东 , 汪思应 . 四逆汤对大鼠心肺复苏后脑组织损伤的影响. 蚌埠医学院学报, 2009, 34(1): 18-20.
[17]	姜翠荣 , 高琴 , 王晓梅 , 李正红 . 不同浓度硝酸甘油对大鼠离体心脏缺血/再灌注损伤的作用. 蚌埠医学院学报, 2011, 36(1): 7-10.
[18]	于影 , 胡杰 , 姜翠荣 , 李正红 , 高琴 . 远距缺血后处理对大鼠急性心肌缺血/再灌注损伤的影响. 蚌埠医学院学报, 2011, 36(2): 109-111,116.
[19]	姚荣英 , 顾璇 , 郑玲 . 瘦素抵抗肥胖雌性大鼠肺通气功能的损伤研究. 蚌埠医学院学报, 2011, 36(11): 1181-1183.
[20]	周玲 , 毛立梅 , 包蔚雷 . 还原型谷胱甘肽预处理对大鼠小肠淤血性损伤的影响. 蚌埠医学院学报, 2012, 36(12): 1418-1420.

点击查看大图

计量

文章访问数: 2879
HTML全文浏览量: 270
PDF下载量: 23
被引次数: 0

锰对大鼠肝脏线粒体氧化损伤的作用机制

申玲
贾克^,

通讯作者: 贾克, 讲师.jake981005@126.com

作者简介: 申玲(1973-),女,实验师.

蚌埠医学院预防医学系, 安徽蚌埠 233030

收稿日期: 2011-04-20

基金项目: 蚌埠医学院自然科学研究资助项目(BY0834)

关键词:

锰 /
肝脏线粒体 /
氧化损伤 /
大鼠

摘要: 目的:观察不同剂量的锰对大鼠肝脏线粒体的氧化损伤作用,探讨其相关机制。方法:将24只雄性SD大鼠随机均分为对照组和MnCl₂低、中、高剂量组,分别腹腔注射生理盐水和2、8、32 g/kg MnCl₂溶液,每天1次,连续30 d后取大鼠肝组织测定线粒体PT孔、线粒体膜肿胀度、线粒体膜电位、琥珀酸脱氢酶(SDH)、细胞色素C、羟自由基(OH·)和谷胱甘肽过氧化物酶(GSH-PX)。结果:各组间肝线粒体PT孔差异均有统计学意义(P<0.01);MnCl₂高剂量组线粒体膜肿胀度小于对照组和MnCl₂低剂量组(P<0.05);MnCl₂高剂量组线粒体膜电位光密度均低于其他3组(P<0.05~P<0.01)。与对照组和MnCl₂低剂量组相比,MnCl₂中、高剂量组肝线粒体SDH均下降(P<0.01),且MnCl₂中、高剂量组间差异亦有统计学意义(P<;与对照组和MnCl₂低剂量组相比,MnCl₂高剂量组肝线粒体细胞色素C上升(P<0.05)。MnCl₂高剂量组肝线粒体OH·显著高于其他3组(P<0.01);与对照组比较,MnCl₂低、中、高剂量组大鼠肝线粒体GSH-PX显著降低(P<0.05)。结论:锰可导致线粒体氧化损伤,引起大鼠肝线粒体PT孔开放、膜电位下降,SDH、GSH-PX降低,细胞色素C、OH·显著升高,对机体产生毒性作用。

English Abstract

The mechanism of manganese induced oxidative damage on rat liver mitochondria

SHEN Ling
JIA Ke^,

Corresponding author: JIA Ke, 讲师.jake981005@126.com

Department of Preventive Medicine, Bengbu Medical College, Bengbu Anhui 233030, China

Received Date: 2011-04-20

Abstract: Objective:To observe the oxidative damage of rat liver mitochondria induced by different doses of manganese and explore the related mechanism. Methods:Twenty four male SD rats were divided into 4 groups,6 rats in each group,including control group,low dose group,medium dose group and high dose group. The rats in control group were injected normal saline intraperitoneally and the rats in low dose, medium and high dose groups were injected 2 g·kg^-1·d^-1, 8 g·kg^-1·d^-1 and 32 g·kg^-1·d^-1 MnCl₂ intraperitoneally respectively for 30 days. The rat liver tissue was extracted and mitochondria suspension was obtained by differential centrifugation separation to measure mitochondrial PT pore,the degree of mitochondrial swelling,the mitochondrial membrane potential and the content of succinate dehydrogenase (SDH), cytochrome C, hydroxyl radical OH·and glutathione peroxidase (GSH-PX). Results:The mitochondrial PT pore in the four groups was different and the differences had statistical significances(P<0.01); the mitochondrial swelling degree in high dose group was lower than that in control and low dose group(P<0.05); the mitochondrial membrane potential in high dose group was decreased compared with that of other groups(P<0.05-P<0.01); the content of SDH in medium and high dose group was decreased compared with that in control and low dose group(P<0.01) and the difference of SDH between medium and high dose group had statistical significance(P<0.01); the cytochrome C content in high dose group was higher than that in control and low dose group(P<0.05); the content of hydroxyl radical OH·in high dose group was increased compared with that in other three groups (P<0.01); in the same time, the content of GSH-PX in low, medium and high groups decreased compared with that in control group(P<0.05). Conclusions:Manganese can induce mitochondrial oxidative damage. Manganese has the toxic effects on rat mitochondria and the toxic effects induce rat liver mitochondrial PT pore opening,decreasing the optical density of membrane potential and the content of SDH and GSH-PX,increasing the content of cytochrome C and hydroxyl radical OH·significantly.