【摘要】：[目的]采用病例對照研究方法,觀察鄰苯二甲酸酯暴露對男童線粒體DNA氧化損傷及線粒體DNA拷貝數(shù)的影響,探索鄰苯二甲酸酯影響男性性發(fā)育的可能機(jī)制。[方法]將2013—2014年經(jīng)上海市某三級甲等醫(yī)院確診為體質(zhì)性發(fā)育遲緩的8~15歲男童納入研究,共48例病例,匹配以同一年齡段同一醫(yī)院就診于外科的正常男童60例作為對照。采用高效液相色譜-串聯(lián)質(zhì)譜法檢測病例和對照男童尿液中鄰苯二甲酸單丁酯(Mn BP)、鄰苯二甲酸甲酯(MMP)、鄰苯二甲酸乙酯(MEP)鄰苯二甲酸(2-乙基己基)單酯(MEHP)、鄰苯二甲酸(2-乙基-5羥基己基)單酯(MEHHP)、鄰苯二甲酸(2-乙基-5氧己基)單酯(MEOHP)濃度。運(yùn)用t檢驗(yàn)及多元線性回歸模型分析鄰苯二甲酸酯水平與線粒體DNA氧化損傷、線粒體DNA拷貝數(shù)在病例和對照中的差異及兩者間的關(guān)聯(lián)。[結(jié)果]病例組男童尿液Mn BP、MMP、MEHP、Sum DEHP濃度顯著高于正常對照組(P值分別為0.017、0.008、0.038、0.020)。病例組男童線粒體DNA拷貝數(shù)高于對照組(P=0.001),兩組線粒體DNA氧化損傷水平差異無統(tǒng)計(jì)學(xué)意義。男童尿液MMP、MEHP、Sum DEHP濃度與線粒體DNA拷貝數(shù)存在顯著正相關(guān)(P0.05),但未發(fā)現(xiàn)線粒體DNA氧化損傷水平與鄰苯二甲酸酯暴露水平間顯著關(guān)聯(lián)。[結(jié)論]體質(zhì)性發(fā)育遲緩男童體內(nèi)鄰苯二甲酸酯暴露水平和線粒體DNA拷貝數(shù)顯著升高,鄰苯二甲酸酯暴露可能是線粒體功能受損的一個危險因素。
[Abstract]:[objective] to observe the effect of phthalate exposure on oxidative damage of mitochondrial DNA and the number of DNA torture in boys by case-control study, and to explore the possible mechanism of phthalate affecting male sexual development. [methods] A total of 48 boys aged 8 years and 15 years old who were diagnosed as physical retardation by a Grade 3A hospital in Shanghai from 2013 to 2014 were enrolled in the study. 60 normal boys who were treated in surgery in the same hospital of the same age group were used as control. High performance liquid chromatography-tandem mass spectrometry was used to determine the concentration of monobutyl phthalate (Mn BP), methyl phthalate (MMP), ethyl phthalate (MEP) phthalic acid (2-ethylhexyl) monoester (MEHP), phthalic acid (2-ethyl-5-hydroxyhexyl) monoester (MEHHP), phthalic acid (2-ethyl-5-oxohexyl) monoester (MEOHP) in the urine of case and control boys. T test and multiple linear regression model were used to analyze the difference between phthalate level and oxidative damage of mitochondrial DNA, the number of DNA copies in cases and controls, and the correlation between them. [results] the urine Mn BP,MMP,MEHP,Sum DEHP concentration in the case group was significantly higher than that in the normal control group (P = 0.017, 0.008, 0.038, 0.020, respectively). The number of mitochondrial DNA copies in the case group was higher than that in the control group (P 鈮，

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