中国地方病学杂志
中國地方病學雜誌
중국지방병학잡지
CHINESE JOURNAL OF ENDEMIOLOGY
2011年
5期
493-497
,共5页
纪春艳%傅春玲%向全永%许松%朱明清%刘建%王大朋%张洁%安艳
紀春豔%傅春玲%嚮全永%許鬆%硃明清%劉建%王大朋%張潔%安豔
기춘염%부춘령%향전영%허송%주명청%류건%왕대붕%장길%안염
砷%内皮,血管%循环内皮祖细胞%效应标志物
砷%內皮,血管%循環內皮祖細胞%效應標誌物
신%내피,혈관%순배내피조세포%효응표지물
Arsenic%Endothelium,vascular%Circulating endothelial progenitor cells%Biomarkers
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、> 50μg/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(O-·2)和炎症反应指标C-反应蛋白(CRP)、一氧化氮(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、67.5 μmol/kg)、O-·2(几何均数分别为4774.6、5143.3、4736.0 U/kg)、CRP[(5.92±2.44)、(5.11±2.40)、(5.55±2.96)mg/L]、NO水平[(659.8±387.5)、(667.4±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(q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。
目的 觀察低砷飲水人群血管內皮損傷早期效應標誌物的改變。方法 在江囌省盱眙縣沿河村,選擇90名噹地居住10年以上的居民作為觀察對象,併根據傢庭飲水含砷量將其分為3組,即< 10、10 ~ 50、> 50μg/L組,分彆為32、28、30人。分彆採用硫代巴比妥痠(TBA)法、比色法、比濁法、硝痠還原酶法檢測觀察對象血漿氧化應激指標丙二醛(MDA)、抗超氧陰離子自由基(O-·2)和炎癥反應指標C-反應蛋白(CRP)、一氧化氮(NO)水平,採用流式細胞術檢測全血中循環內皮祖細胞(CEPCs)數量。結果 <10、10 ~ 50、>50μg/L組間血漿MDA(幾何均數分彆為61.1、65.5、67.5 μmol/kg)、O-·2(幾何均數分彆為4774.6、5143.3、4736.0 U/kg)、CRP[(5.92±2.44)、(5.11±2.40)、(5.55±2.96)mg/L]、NO水平[(659.8±387.5)、(667.4±486.6)、(762.1±763.2)μmol/kg]比較,差異均無統計學意義(F值分彆為0.00、0.46、0.80、0.47,P均>0.05)。各組CEPCs數量(中位數分彆為0.96×10-5、0.77×10-5、1.59×10-5)比較,差異有統計學意義(F=5.08,P< 0.05),其中<10、10~50μg/L組明顯低于>50μg/L組(q值分彆為4.58、6.65,P均<0.05)。結論 低砷暴露人群在尚未齣現明顯的氧化應激損傷及炎癥改變情況下,體內CEPCs水平隨水砷明顯變化,提示低砷暴露人群可能存在血管內皮損傷。
목적 관찰저신음수인군혈관내피손상조기효응표지물적개변。방법 재강소성우이현연하촌,선택90명당지거주10년이상적거민작위관찰대상,병근거가정음수함신량장기분위3조,즉< 10、10 ~ 50、> 50μg/L조,분별위32、28、30인。분별채용류대파비타산(TBA)법、비색법、비탁법、초산환원매법검측관찰대상혈장양화응격지표병이철(MDA)、항초양음리자자유기(O-·2)화염증반응지표C-반응단백(CRP)、일양화담(NO)수평,채용류식세포술검측전혈중순배내피조세포(CEPCs)수량。결과 <10、10 ~ 50、>50μg/L조간혈장MDA(궤하균수분별위61.1、65.5、67.5 μmol/kg)、O-·2(궤하균수분별위4774.6、5143.3、4736.0 U/kg)、CRP[(5.92±2.44)、(5.11±2.40)、(5.55±2.96)mg/L]、NO수평[(659.8±387.5)、(667.4±486.6)、(762.1±763.2)μmol/kg]비교,차이균무통계학의의(F치분별위0.00、0.46、0.80、0.47,P균>0.05)。각조CEPCs수량(중위수분별위0.96×10-5、0.77×10-5、1.59×10-5)비교,차이유통계학의의(F=5.08,P< 0.05),기중<10、10~50μg/L조명현저우>50μg/L조(q치분별위4.58、6.65,P균<0.05)。결론 저신폭로인군재상미출현명현적양화응격손상급염증개변정황하,체내CEPCs수평수수신명현변화,제시저신폭로인군가능존재혈관내피손상。
Objective To observes the change of early effective biomarkers of endothelial injury with lowarsenic exposure in drinking water. Methods Ninety rurad 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(O-·2),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), O-·2 (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 x 10-5, 0.77 x 10-5,1.59 x 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.