燃煤砷暴露对人体红细胞免疫黏附功能受损机制的探讨  

Exploration on impaired mechanism of human red cell immune adherence function by arsenic exposure

作　　者：刘大维[1] 张碧霞 张爱华[3] 

机构地区：[1]辽宁省锦州市疾病预防控制中心,辽宁锦州121000 [2]贵州省贵阳市解放军四十四医院,贵阳550000 [3]贵州省贵阳医学院公共卫生学院,贵阳550004

出　　处：《中国卫生检验杂志》2012年第5期1049-1050,1056,共3页Chinese Journal of Health Laboratory Technology

摘　　要：目的:通过对燃煤型砷中毒患者红细胞免疫黏附功能相关指标的检测,探讨其红细胞免疫黏附功能损伤的可能机制。方法:采用ELISA法测定红细胞CR1(RBC-CR1)分子数量及PCR-RFLP法测定CR1密度基因多态性。结果:砷中毒组RBC-CR1密度基因多态性分布情况:HH型72例(70%)、HL型27例(26.2%)、LL型4例(3.8%)。砷中毒患者RBC-CR1分子数量及各基因型CR1分子数量均明显低于健康对照组,差异均有统计学意义(P<0.01)。结论:RBC-CR1数量减少可能是砷中毒引起红细胞免疫黏附功能受损的重要机制。Objective：To explore the possible mechanism of immune adherence function damage of erythrocytes in arsenism patients.Methods： The number of CR1 was detected by ELISA.RBC-CR1 genomic density polymorphism was detected by PCR-RFLP.Results： The RBC-CR1 genonic density polymorphism distribution state was type HH（70%）,HL（26.2%）and LL（3.8%） in arsenism patients;RBC-CR1 number and CR1 number in different genotypes in arsenism patients were all lower than those in controls,the difference had statistical significance（P〈0.01）.Conclusion： Decrease in RBC-CR1 may be the main mechanism to cause immune adherence function damage of red cells.

关 键 词：燃煤砷暴露 人体 红细胞 CR1 基因多态性 

分 类 号：R595[医药卫生—内科学]