Genetic polymorphism of GSTM1 and antioxidant supplementation influence lung function in relation to ozone exposure in asthmatic children in Mexico City.

Genetic polymorphism of GSTM1 and antioxidant supplementation influence lung function in relation to ozone exposure in asthmatic children in Mexico City.
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发表时间:
2004
期刊:
影响因子:
10
通讯作者:
I. Romieu;S. Jj;Matiana Ramírez-Aguilar;H. Moreno-Macías;N. I. Reyes-Ruiz;B. D. Río-Navarro;M. Hernández-Ávila;S. London
I. Romieu;S. Jj;Matiana Ramírez-Aguilar;H. Moreno-Macías;N. I. Reyes-Ruiz;B. D. Río-Navarro;M. Hernández-Ávila;S. London
中科院分区:
医学1区
文献类型:
--
作者:
I. Romieu;S. Jj;Matiana Ramírez-Aguilar;H. Moreno-Macías;N. I. Reyes-Ruiz;B. D. Río-Navarro;M. Hernández-Ávila;S. London

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背景我们最近报道,在墨西哥城臭氧暴露较高的地区,补充抗氧化剂维生素C和维生素E可以缓解158名哮喘儿童与臭氧相关的用力呼气流量(FEF(25-75))的下降。方法检测氧化应激应答基因谷胱甘肽S转移酶M1(GSTM1零基因)的缺失是否影响FEF(25-75)臭氧相关性下降和补充抗氧化剂的益处。结果服用安慰剂的GSTM1缺失儿童的FEF(25-75)显著降低(每50 ppb臭氧的百分比变化2.9(95%CI-5.2~-0.6),p=0.01),而GSTM1阳性儿童则没有。相反,在GSTM1基因缺失的儿童中,抗氧化剂的作用更强。结论GSTM1基因缺陷的哮喘儿童可能更容易受到臭氧对小气道的有害影响,补充抗氧化剂可能会获得更大的好处。
BACKGROUND We recently reported that antioxidant supplementation with vitamins C and E mitigated ozone related decline in forced expiratory flow (FEF(25-75)) in 158 asthmatic children in an area with high ozone exposure in Mexico City. METHODS A study was undertaken to determine whether deletion of glutathione S-transferase M1 (GSTM1 null genotype), a gene involved in response to oxidative stress, influences ozone related decline in FEF(25-75) and the benefit of antioxidant supplementation. RESULTS GSTM1 null children receiving placebo had significant ozone related decrements in FEF(25-75) (percentage change per 50 ppb of ozone 2.9 (95% CI -5.2 to -0.6), p=0.01); GSTM1 positive children did not. Conversely, the effect of antioxidants was stronger in children with the GSTM1 null genotype. CONCLUSIONS Asthmatic children with a genetic deficiency of GSTM1 may be more susceptible to the deleterious effects of ozone on the small airways and might derive greater benefit from antioxidant supplementation.