Franko Alenka, Dodic-Fikfak Metoda, Arnerić Niko, Dolzan Vita
Clinical Institute of Occupational Medicine, University Medical Centre, Ljubljana, Slovenia.
J Biomed Biotechnol. 2009;2009:493083. doi: 10.1155/2009/493083. Epub 2009 Jul 14.
Manganese and extracellular superoxide dismutases (SOD2 and SOD3) are part of the enzymatic defence against reactive oxygen species, which are involved in the pathogenesis of asbestosis. This study investigates whether SOD2Ala - 9Val and SOD3 Arg213Gly genetic polymorphisms represent risk factors for asbestosis in workers exposed to asbestos. The study included 262 cases with asbestosis and 265 controls with no asbestos-related disease. Cumulative asbestos exposure was calculated for each subject. A real-time PCR assay was introduced for genotyping. Logistic regression analysis was used to assess asbestosis risk. Asbestosis was associated with the homozygous SOD2 - 9Ala/Ala genotype (OR = 1.50, 95% CI 1.01-2.24), whereas the association for the SOD3 Arg/Gly genotype was not significant (OR = 1.63, 95% CI 0.62-4.27). The finding that the SOD2 - 9Ala/Ala genotype increases the risk for asbestosis indicates that, in addition to asbestos exposure, genetic factors may also have a significant influence on the development of asbestosis.
锰和细胞外超氧化物歧化酶(SOD2和SOD3)是针对活性氧的酶防御机制的一部分,活性氧参与了石棉肺的发病过程。本研究调查SOD2 Ala - 9Val和SOD3 Arg213Gly基因多态性是否是接触石棉工人患石棉肺的危险因素。该研究纳入了262例石棉肺患者和265例无石棉相关疾病的对照。计算了每个受试者的累积石棉暴露量。采用实时聚合酶链反应检测法进行基因分型。使用逻辑回归分析评估石棉肺风险。石棉肺与纯合子SOD2 - 9Ala/Ala基因型相关(比值比=1.50,95%置信区间1.01 - 2.24),而SOD3 Arg/Gly基因型的相关性不显著(比值比=1.63,95%置信区间0.62 - 4.27)。SOD2 - 9Ala/Ala基因型增加石棉肺风险这一发现表明,除了石棉暴露外,遗传因素可能也对石棉肺的发生有显著影响。