低砷饮水人群血管内皮损伤早期效应标志物的观察

Biomarkers of early vascular endothelial injury with low-arsenic exposure in drinking water

目的观察低砷饮水人群血管内皮损伤早期效应标志物的改变。方法在江苏省盱眙县沿河村，选择90名当地居住10年以上的居民作为观察对象，并根据家庭饮水含砷量将其分为3组，即〈10、10～50、〉50ug／L组，分别为32、28、30人。分别采用硫代巴比妥酸（TBA）法、比色法、比浊法、硝酸还原酶法检测观察对象血浆氧化应激指标丙二醛（MDA）、抗超氧阴离子自由基（01）和炎症反应指标C-反应蛋白（CRP）、-氧化氮（NO）水平，采用流式细胞术检测全血中循环内皮祖细胞（CEPCs）数量。结果〈10、10～50、〉50μg／L组间血浆MDA（几何均数分别为61．1、65．5、67．5μmoL／kg）、O2（几何均数分别为4774．6、5143．3、4736．0U／kg）、CRP[（5．92±2．44）、（5．11±2．40）、（5．55±2．96）mg／L]、N0．水平[（659．8±387．5）、（667．44-486．6）、（762．1±763．2）μmol／kg]比较，差异均无统计学意义（F值分别为0．00、0．46、0．80、0．47，P均〉0．05）。各组CEPCs数量（中位数分别为0．96×10^-5、0．77×10^-5、1．59×10^-5）比较，差异有统计学意义（F=5．08，P〈0．05），其中〈10、10—50μg/L组明显低于〉50μg／L组（g值分别为4．58、6．65，P均〈0．05）。结论低砷暴露人群在尚未出现明显的氧化应激损伤及炎症改变情况下，体内CEPCs水平随水砷明显变化，提示低砷暴露人群可能存在血管内皮损伤。

Objective To observes the change of early effective biomarkers of endothelial injury with low- arsenic exposure in drinking water. Methods Ninety rural residents, who had lived in Yanhe village, Xuyi county and Jiangsu province for at least 10 years, were recruited by simple random sampling in this study. The level of arsenic in their household shallow well were divided into three groups, which were 〈 10 （32 people）, 10 - 50（28 people） and 〉 50 μg/L（30 people）. Blood samples from individuals were collected. Malondialdehyde（MDA） in human plasma, which is considered as the most important marker for monitoring lipid peroxidation, was determined as conjugate with tetrabutylammonium hydrogen sulphate （TBA）. The level of anti-superoxide anion radical （OF）, C-reactive protein （CRP） and NO in human plasma was measured with colorimetry, turbidimetry and nitric acid reductase, respectively. The number of circulating endothelial progenitor cells（CEPCs） in peripheral blood was analyzed by CD133~/KDR~ antibodies and flow cytometry. Results Ninety cases underwent questionnaires. Between the groups, the difference of the levels of MDA（61.1, 65.5, 67.5 μmol/kg）, O2（4774.6, 5143.3, 4736.0 U/kg）, CRP[ （5.92 ±2.44）, （5.11 ± 2.40）, （5.55 ± 2.96）mg/L], and NO[ （659.8 ± 387.5）, （667.4 ± 486.6）, （762.1 ±763.2）μmol/kg], was not statistically significant （F = 0.00, 0.46, 0.80, 0.47, all P 〉 0.05）. The difference of the number of CEPCs in different groups of arsenic in drinking water was statistically significant（0.96 × 10^-5, 0.77 × 10^-5, 1.59 × 10^-5, F = 5.08, P 〈 0.05）, where 〈 10, 10 - 50 μg/L groups were significantly lower than 〉 50 μg/L group （q = 4.58, 6.65, all P 〈 0.05）. Conclusions The number of CEPCs in peripheral blood changes significantly with lower-arsenic exposure, whereas there are no obvious changes with the markers of oxidized damage and inflammation. This is the first human demonstration showing that lower-arsenic exposure may cause endothelial injury.