十溴二苯乙烷暴露诱导小鼠氧化应激反应  

Decabromodiphenyl ethane exposure induced oxidative stress in mice

作　　者：冀禹彤 周淑馨 李振民 姜玟 齐凯歌 胡庭俊[1] 于美玲 Ji Yutong;Zhou Shuxin;Li Zhenmin;Jiang Wen;Qi Kaige;Hu Tingjun;Yu Meiing(College of Animal Science and Technology,Guangxi University,Guangxi Nanning 530004)

机构地区：[1]广西大学动物科学技术学院,广西南宁530004

出　　处：《现代畜牧兽医》2023年第3期1-6,共6页Modern Journal of Animal Husbandry and Veterinary Medicine

基　　金：广西壮族自治区大学生创新创业训练计划项目(S202110593150)。

摘　　要：研究旨在明确十溴二苯乙烷(DBDPE)对小鼠氧化应激的影响。将60只小鼠随机分为5组,连续28 d暴露于0 (D0组,即空白对照组)、5 (D5组)、50 (D50组)、500 mg/(kg·d) bw的DBDPE (D500组)及50 mg/(kg·d) bw DBDPE联合50 mg/(kg·d) bw十溴联苯醚(B50+D50组)中。结果显示,与D0组相比,D500组和B50+D50组小鼠血清中丙二醛(MDA)含量均极显著下降(P<0.01),D50组小鼠血清中乳酸脱氢酶(LDH)活性显著下降(P<0.05);D50组小鼠肝脏组织中MDA含量极显著升高(P<0.01),D5组与D500组肝脏MDA含量显著下降(P<0.05)。与D0组相比,D5组、D500组与B50+D50组小鼠肝脏中过氧化氢酶(CAT)活性均显著降低(P<0.01);D50组、D500组与B50+D50组小鼠肝脏中超氧化物歧化酶(SOD)活性均极显著升高(P<0.01),D500组与B50+D50组小鼠肝脏中微量还原型谷胱甘肽(GSH)含量均极显著升高(P<0.01);D500组小鼠肝脏中谷胱甘肽-S转移酶(GSH-ST)活性极显著升高(P<0.01)。与D0组相比,D500组小鼠肾脏组织中MDA含量极显著升高(P<0.01);各染毒组小鼠肾脏组织中CAT活性均极显著下降(P<0.01);D50组和D500组小鼠肾脏中SOD活性均极显著升高(P<0.01);B50+D50组小鼠肾脏中GSH含量极显著升高(P<0.01);D5组和D500组小鼠肾脏中GSH-ST活性显著升高(P<0.05)。研究表明,DBDPE暴露可通过下调CAT活性和上调SOD活性破坏小鼠体内氧化还原稳态,诱导小鼠肝脏和肾脏氧化应激损伤,导致肝肾毒性作用,其中500 mg/kg DBDPE对机体氧化还原系统影响较大。The aim of the study was to determine the effects of decabromodiphenyl ethane(DBDPE) on oxidative stress in mice. Sixty mice were randomly divided into five groups and exposed to 0(D0 group, blank control group), 5(D5 group),50(D50 group), 500 mg/(kg·d) bw DBDPE(D500 group) and 50 mg/(kg·d) bw DBDPE combined with 50 mg/(kg·d) bw decabromodiphenyl ether(B50+D50 group). The results showed that compared with D0 group, MDA content in serum of D500 group and B50+D50 group was extremely decreased(P<0.01), and LDH activity in serum of D50 group was significantly decreased(P<0.05). MDA content in liver tissues of mice in D50 group was extremely increased(P<0.01),while MDA content in liver of D5 group and D500 group was significantly decreased(P<0.05). Compared with D0 group,CAT activity in liver of D5 group, D500 group and B50+D50 group were significantly decreased(P<0.05). SOD activity in liver of D50 group, D500 group and B50+D50 group was extremely increased(P<0.01), GSH content in liver of D500 group and B50+D50 group was extremely increased(P<0.01), the activity of GSH-ST in liver of D500 group was extremely increased(P<0.01). Compared with D0 group, MDA content in kidney tissue of mice in D500 group was extremely increased(P<0.01). The activity of CAT in kidney tissue of mice in all infected groups was extremely decreased(P<0.01). SOD activity in kidney of D50 group and D500 group was extremely increased (P<0.01). The content of GSH in kidney of B50+D50 group was extremely increased(P<0.01), the activity of GSH-ST in kidney of D5 group and D500 group was significantly increased(P<0.05). The study indicates that DBDPE exposure can damage REDOX homeostasis in mice by down-regulating CAT activity and up-regulating SOD activity, induce oxidative stress injury in liver and kidney, and lead to hepatorenal toxicity. Among them, 500 mg/kg DBDPE has a greater impact on the body’s redox system.

关 键 词：十溴二苯乙烷(DBDPE) 小鼠 氧化应激 肝脏 肾脏 

分 类 号：S859.53[农业科学—临床兽医学]