人体血液红细胞对外源性甲醛氧化能力转移作用的体外研究  

An in vitro study on carrier-like function of human erythrocytes for transferring carbonyl of exogenous formaldehyde molecule

作　　者：梅宇飞[1] 魏晨曦[1] 刘志敏[1] 陈绍恢[1] 曹凤华[1] 杨旭[1] 

机构地区：[1]华中师范大学生命科学学院遗传调控与整合生物学湖北省重点实验室,湖北武汉430079

出　　处：《环境与健康杂志》2014年第2期107-110,共4页Journal of Environment and Health

基　　金：国家自然科学基金重点项目(51136002);"十二五"国家科技支撑计划重点项目(2012BAJ02B0301)

摘　　要：目的探讨人体血液红细胞对外源性甲醛的缓冲作用,外源性甲醛对红细胞的氧化损伤作用以及氧化损伤的红细胞对外源性甲醛分子具有氧化能力转移作用。方法以健康人血为研究对象,分别向4组反应体系(纯水、生理盐水、血浆、全血)中加入不同浓度的甲醛溶液使之终浓度为0、0.03、0.05、0.125、0.25、0.5、1、2、4、8、16 mg/L。37℃水浴1 h后,采用AHMT法检测加入外源性甲醛后4组溶液中的甲醛浓度,并检测加入外源性甲醛后血液中红细胞膜蛋白羰基化值及血浆丙二醛(MDA)含量。结果生理盐水及纯水对外源性甲醛无缓冲作用,血浆在甲醛浓度≤2.5 mg/L时,具有缓冲作用,全血即使在高浓度甲醛(16 mg/L)下也具有缓冲作用。当甲醛浓度≥0.25 mg/L时,红细胞膜蛋白羰基化值高于对照组,差异有统计学意义(P<0.05);当甲醛浓度≥0.03 mg/L时,MDA值高于对照组,差异有统计学意义(P<0.05)。结论血液对外源性甲醛具有缓冲作用且发挥主要作用的为红细胞,较高浓度的甲醛(≥0.25mg/L)会对红细胞产生氧化损伤作用,而红细胞则起到对外源性甲醛分子氧化能力转移作用,提示羰基化红细胞可能是甲醛远距离毒性的载体。Objective To investigate whether blood has a buffering function on exogenous formaldehyde （FA）, exogenous FA induced oxidative damage in erythrocytes and the oxidative erythrocytes act as the carrier-like function for transferring carbonyl of exogenous FA molecule. Methods Healthy human blood was taken as the experimental material. Different concentrations of FA were added in four groups （double distilled water, saline, plasma, whole blood）. After one hour of water bath at 37 ℃, the concentration of FA was measured with AHMT method. The carbonylation value of erythrocyte membrane protein in the blood and MDA content of plasma were determined. Results Saline and doubled distilled water did not present buffering function on exogenous FA while plasma had buffering function when concentration of FA was less than 2.5 mg/L, whole blood had buffering function even at the dose of 16 mg/L. When the concentration of FA exceeded 0.25 mg/L, the carbonylation value of erythrocyte membrane protein was significant different compared with that of the control group （P〈0.05）. When the concentration of FA exceeded 0.03 mg/L, MDA content was extremely significant different compared with the control group （P〈O.O1）. Conclusion Blood has buffering function on exogenous FA and the major role is erythrocytes. High concentration of FA （≥0.25 mg/L） can cause oxidative damage in erythrocytes, while the erythrocytes act as the carrier-like function for transferring carhonyl of exogenous FA molecule, which indicates that the carbonylation of erythrocytes may act as the carrier for FA distant-site toxicity.

关 键 词：甲醛 血液 红细胞 氧化应激 

分 类 号：R994.6[医药卫生—毒理学]