氟、砷中毒小鼠肝亚细胞器脂质过氧化损害  

Lipid peroxidation injuries of hepatic subcellular fractions in mice caused by chronic fluorsis,arsenism poisoning

作　　者：刘起展[1] 黄厚今[1] 董国宾[1] 周远忠[1] 王建华[1] 胡斌丽[1] 李红[1] 赵曼平[1] 

机构地区：[1]贵州省遵义医学院预防医学教研室,563003

出　　处：《中国公共卫生》2003年第9期1050-1051,共2页Chinese Journal of Public Health

基　　金：贵州省科委自然基金资助 (98- 30 52 );贵州省教委科研基金资助 (2 0 0 0 51 8)

摘　　要：目的　探讨慢性氟中毒、砷中毒及联合中毒对小鼠肝亚细胞器的脂质过氧化损害程度。方法　昆明系小白鼠 12 0只 ,随机分成对照、氟中毒、砷中毒和氟砷联合中毒 4组 ,分别自由进食普通、高氟、高砷和高氟高砷饲料 ,饲养 6个月和 12个月。分离出肝线粒体和微粒体 ,分别检测其LPO含量、SDHase和G - 6 -Pase活性。结果　 3种中毒均可引起肝线粒体和微粒体LPO含量显著升高 ,线粒体标志酶SDHase活性和微粒体标志酶G - 6 -Pase活性均显著降低 ,各亚细胞器LPO含量升高分别与其相应标志酶活性降低存在显著的负相关关系 ,但 3种中毒对这些指标的影响程度不同。结论　慢性氟中毒、砷中毒和氟砷联合中毒均能引起肝亚细胞器线粒体和微粒体发生脂质过氧化损害作用 ,并且氟、砷毒物对这一作用存在一定的相互影响。Objective To study the levels,similarities and differences of the lipid peroxidation injury effects in hepatic subcellular fractions caused by chronic fluorosis,arsenism and fluoride-arsenic poisoning respectively in mice.Methods 120 mice were randomly divided into four groups which were fed with four different diets supplemented respectively fluoride arsenic and fluoride-arsenic for 6 and 12 months.The LPO contents in hepatic mitochondria and microsomes and the activities of SDHase in hepatic mitochondria and G-6-Pase in hepatic microsomes were determined.Results In the three poisoning groups:the LPO contents in hepatic mitochondria and microsomes were significally increased.The activities of SDHase in hepatic mitochondria and G-6-Pase in hepatic microsomes were markedly decreased.The increases of LPO contents in two subcellular fractions showed significally negative correlation to the decreases of their enzymes activities,respectively.However,the effect of the three diffierent poisons on these indices were different.Conclusion In mice,the lipid peroxidation injuries in hepatic mitochondria and microsomes were caused by the chronic three poisons,to some extent,fluoride and arsenic can influence the effect together.

关 键 词：氟中毒 砷中毒 氟砷联合中毒 脂质过氧化 肝 亚细胞器 

分 类 号：R599.9[医药卫生—内科学]