Congenital heart defects and maternal biomarkers of oxidative stress.

Congenital heart defects and maternal biomarkers of oxidative stress.
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DOI:
10.1093/ajcn.82.3.598
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发表时间:
2005-09
期刊:
The American journal of clinical nutrition
影响因子:
--
通讯作者:
Charlotte A. Hobbs;Mario A. Cleves;Weizhi Zhao;S. Melnyk;S. James
Charlotte A. Hobbs;Mario A. Cleves;Weizhi Zhao;S. Melnyk;S. James
中科院分区:
其他
文献类型:
--
作者:
Charlotte A. Hobbs;Mario A. Cleves;Weizhi Zhao;S. Melnyk;S. James

文献摘要

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背景:受非综合征性先天性心脏病影响的孕妇,其同型半胱氨酸-蛋氨酸途径发生改变,这可能表明氧化应激暴露增加或抗氧化防御能力降低或两者兼而有之。目的:我们的目标是建立一个非综合征性先天性心脏病的母体代谢风险概况,以加强目前的预防策略。设计:采用病例对照设计,我们测量了转硫途径的生物标志物,以人群为基础的样本的妇女,其妊娠受先天性心脏病(331例)和对照组的妇女(125名对照)。在调整生活方式和社会人口学变量后,比较病例组和对照组的还原型和氧化型谷胱甘肽、维生素B-6、同型半胱氨酸、半胱氨酸、半胱氨酰甘氨酸(CysGly)和谷氨酰半胱氨酸(GluCys)的血浆浓度。结果经协变量校正后,病例组血浆还原型谷胱甘肽(P < 0.0001)、GluCys(P < 0.0001)和维生素B-6(P = 0.0023)的平均浓度显著低于对照组,而同型半胱氨酸(P < 0.0001)和氧化型谷胱甘肽(P < 0.0001)的平均浓度显著高于对照组。结论:与无先天性心脏病史的孕妇相比,有先天性心脏病史的孕妇体内涉及转硫途径的氧化应激生物标志物明显更高。需要进一步分析氧化应激的相关生物标志物以及遗传和环境因素,以确定观察到的变化的基础。确定氧化应激生物标志物改变的性质和程度可能会建议主要干预策略,并为更好地了解先天性心脏病的发病机制提供线索。
BACKGROUND Women who have had pregnancies that were affected by nonsyndromic congenital heart defects have alterations in the homocysteine-methionine pathway that may indicate increased exposure to oxidative stress or reduced antioxidant defense or both. OBJECTIVE Our goal was to establish a maternal metabolic risk profile for nonsyndromic congenital heart defects that would enhance current preventive strategies. DESIGN Using a case-control design, we measured biomarkers of the transsulfuration pathway in a population-based sample of women whose pregnancies were affected by congenital heart defects (331 cases) and in a control group of women (125 controls). Plasma concentrations of reduced and oxidized glutathione, vitamin B-6, homocysteine, cysteine, cysteinylglycine (CysGly), and glutamylcysteine (GluCys) were compared between cases and controls after adjustment for lifestyle and sociodemographic variables. RESULTS After covariate adjustment, cases had significantly lower mean plasma concentrations of reduced glutathione (P < 0.0001), GluCys (P < 0.0001), and vitamin B-6 (P = 0.0023) and significantly higher mean concentrations of homocysteine (P < 0.0001) and oxidized glutathione (P < 0.0001) than did controls. CONCLUSIONS Biomarkers of oxidative stress involved in the transsulfuration pathway were significantly higher in women with pregnancies affected by congenital heart defects than in women without such a history. Further analysis of relevant biomarkers of oxidative stress and genetic and environmental factors is required to define the basis for the observed alterations. Identifying the nature and extent of alterations in biomarkers of oxidative stress may suggest primary intervention strategies and provide clues to a greater understanding of the pathogenesis of congenital heart defects.