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首页> 外文期刊>International Journal of Environmental Research and Public Health >Oxidative Stress-Related Genetic Variants May Modify Associations of Phthalate Exposures with Asthma
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Oxidative Stress-Related Genetic Variants May Modify Associations of Phthalate Exposures with Asthma

机译：氧化应激相关的遗传变异可能会改变邻苯二甲酸酯暴露与哮喘的关联。

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Background: Phthalate exposure may increase the risk of asthma. Little is known about whether oxidative-stress related genes may alter this association. First, this motivated us to investigate whether genetic polymorphisms of the oxidative-stress related genes glutathione S -transferase Mu 1 ( GSTM1 ), glutathione S -transferase pi 1 ( GSTP1 ), superoxide dismutase 2 ( SOD2 ), catalase ( CAT ), myeloperoxidase ( MPO ), and EPHX1 in children are associated with phthalate urine concentrations. Second, we addressed the question whether these genes may affect the influence of phthalates on asthma. Methods: In a case-control study composed of 126 asthmatic children and 327 controls, urine phthalate metabolites (monoethyl phthalate (MEP), monobutyl phthalate (MBP), monobenzyl phthalate (MBzP), and mono(2-ethyl-5-hydroxyhexyl)phthalate (MEHHP) were measured by UPLC-MS/MS at age 3. Genetic variants were analyzed by TaqMan assay. Information on asthma and environmental exposures was also collected. Analyses of variance and logistic regressions were performed. Results: Urine MEHHP levels were associated with asthma (adjusted OR 1.33, 95% CI (1.11–1.60). Children with the GSTP1 (rs1695) AA and SOD2 (rs5746136) TT genotypes had higher MEHHP levels as compared to GG and CC types, respectively. Since only SOD2 TT genotype was significantly associated with asthma (adjusted OR (95% CI): 2.78 (1.54–5.02)), we estimated whether SOD2 variants modify the association of MEHHP levels and asthma. As MEHHP concentrations were dependent on GSTP1 and SOD2 , but the assessment of interaction requires independent variables, we estimated MEHHP residuals and assessed their interaction, showing that the OR for SOD2 TT was further elevated to 3.32 (1.75–6.32) when the residuals of MEHHP were high. Conclusions: Urine phthalate metabolite concentrations are associated with oxidative-stress related genetic variants. Genetic variants of SOD2 , considered to be reflect oxidative stress metabolisms, might modify the association of phthalate exposure with asthma.
机译：背景：邻苯二甲酸酯暴露可能会增加哮喘的风险。关于氧化应激相关基因是否可以改变这种关联还知之甚少。首先，这促使我们研究氧化应激相关基因谷胱甘肽S-转移酶Mu 1（GSTM1），谷胱甘肽S-转移酶pi 1（GSTP1），超氧化物歧化酶2（SOD2），过氧化氢酶（CAT），髓过氧化物酶的遗传多态性（MPO）和儿童EPHX1与邻苯二甲酸盐尿液浓度相关。其次，我们解决了这些基因是否可能影响邻苯二甲酸盐对哮喘的影响的问题。方法：在一项由126名哮喘儿童和327名对照组成的病例对照研究中，尿邻苯二甲酸酯代谢物（邻苯二甲酸单乙酯（MEP），邻苯二甲酸单丁酯（MBP），邻苯二甲酸单苄基酯（MBzP）和单（2-乙基-5-羟基己基）在3岁时通过UPLC-MS / MS测定邻苯二甲酸酯（MEHHP），通过TaqMan分析法分析遗传变异，收集哮喘和环境暴露信息，并进行方差分析和logistic回归分析。哮喘（调整后的OR为1.33，95％CI（1.11-1.60））GSTP1（rs1695）AA和SOD2（rs5746136）TT基因型的儿童MEHHP水平分别高于GG和CC类型，因为只有SOD2 TT基因型与哮喘显着相关（校正OR（95％CI）：2.78（1.54–5.02）），我们估计SOD2变体是否改变了MEHHP水平与哮喘的相关性，因为MEHHP浓度取决于GSTP1和SOD2，但评估互动要求自变量，我们估计了MEHHP残差并评估了它们之间的相互作用，表明当MEHHP残差很高时，SOD2 TT的OR进一步提高到3.32（1.75-6.32）。结论：尿中邻苯二甲酸酯代谢物浓度与氧化应激相关的遗传变异有关。 SOD2的遗传变异被认为反映了氧化应激代谢，可能会改变邻苯二甲酸酯暴露与哮喘的关联。

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