BACKGROUND: Age-related macular degeneration (AMD) is a primary cause of blindness among the elderly in developed countries. The nature of AMD is complex and includes both environmental and hereditary factors. Oxidative stress is thought to be essential in AMD pathogenesis. Iron is suggested to be implicated in the pathogenesis of AMD through the catalysis of the production of reactive oxygen species, which can damage the retina. Heme oxygenase-2 is capable of degradation of heme producing free iron ions, thus, diversity in heme oxygenase-2 gene may contribute to AMD. In the present work we analyzed the association between the c.544G>A polymorphism of the heme oxygenase-2 gene (HMOX2) (rs1051308) and AMD. MATERIAL/METHODS: This study enrolled 276 AMD patients and 105 sex- and age-matched controls. Genotyping of the polymorphism was performed with restriction fragment length polymorphism polymerase chain reaction (RFLP-PCR) on DNA isolated from peripheral blood. RESULTS: We did not find any association between the genotypes of the c.544G>A polymorphism and the occurrence of AMD. This lack of association was independent of potential AMD risk factors: tobacco smoking, sex and age. Moreover, we did not find any association between AMD and smoking in our study population. CONCLUSIONS: The results suggest that the c.544G>A polymorphism of the heme oxygenase-2 gene is not associated with AMD in this Polish subpopulation.
Lack of association between the c.544G>A polymorphism of the heme oxygenase-2 gene and age-related macular degeneration.
血红素加氧酶-2基因c.544G>A多态性与年龄相关性黄斑变性之间缺乏关联
阅读:6
作者:Wysokinski Daniel, Synowiec Ewelina, Chmielewska Marta, Wozniak Katarzyna, Zaras MaÅgorzata, Sklodowska Anna, Blasiak Janusz, Szaflik Jerzy, Szaflik Jacek Pawel
| 期刊: | Medical Science Monitor | 影响因子: | 2.100 |
| 时间: | 2011 | 起止号: | 2011 Aug;17(8):CR449-455 |
| doi: | 10.12659/msm.881906 | 研究方向: | 免疫/内分泌 |
特别声明
1、本页面内容包含部分的内容是基于公开信息的合理引用;引用内容仅为补充信息,不代表本站立场。
2、若认为本页面引用内容涉及侵权,请及时与本站联系,我们将第一时间处理。
3、其他媒体/个人如需使用本页面原创内容,需注明“来源:[生知库]”并获得授权;使用引用内容的,需自行联系原作者获得许可。
4、投稿及合作请联系:info@biocloudy.com。
