title: Frequency of polymorphism -262 c/t in catalase gene and oxidative damage in Slovak children with bronchial asthma.
abstract: BACKGROUND
  Bronchial asthma is a complex disease in which genetic factors, environmental factors and oxidative damage are responsible for the initiation and modulation of disease progression. If antioxidant mechanisms fail, reactive oxygen species damage the biomolecules followed by progression of the disease. Catalase is one of the most important endogenous enzymatic antioxidants. In the present study, we examined the hypothesis that increased oxidative damage and polymorphism in the CAT gene (-262 promoter region, C/T) are associated with childhood bronchial asthma.
  
  
  METHODS
  Genotyping of the polymorphisms in the CAT gene in healthy (249) and asthmatic children (248) was performed using polymerase chain reaction-restriction fragment length polymorphism. Markers of oxidative damage: content of sulfhydryl groups and thiobarbituric acid-reactive substances were determined by spectrophotometry in children.
  
  
  RESULTS
  The TT genotype of catalase was more frequent among the asthmatic patients (22.6%) than in healthy children (4.8%) (odds ratio=5.63; 95% confidence interval=2.93-10.81, P<.001). The amount of sulfhydryl groups decreased significantly and conversely, the content of thiobarbituric acid-reactive substances increased significantly in bronchial asthma and in catalase TT genotype compared to other catalase genotypes of this gene.
  
  
  CONCLUSIONS
  These results suggest that catalase polymorphism might participate in development of bronchial asthma and in enhanced oxidative damage in asthmatic children. Genetic variation of enzymatic antioxidants may modulate disease risk.
authors.affiliation: Department of Medical Biochemistry, Jessenius Faculty of Medicine, Comenius University de Bratislava, Martin, República Eslovaca. Electronic address: babusikova@jfmed.uniba.sk.
authors.forename: Eva
authors.initials: E
authors.lastname: Babusikova
authors.forename: Milos
authors.initials: M
authors.lastname: Jesenak
authors.forename: Andrea
authors.initials: A
authors.lastname: Evinova
authors.forename: Peter
authors.initials: P
authors.lastname: Banovcin
authors.forename: Dusan
authors.initials: D
authors.lastname: Dobrota
mesh_terms: D000293:Adolescent; D001249:Asthma / Q000453:epidemiology / Q000235:genetics* / Q000378:metabolism; D001798:Blood Proteins / Q000737:chemistry; D001944:Breath Tests; D002374:Catalase / Q000235:genetics*; D002648:Child; D005260:Female; D005541:Forced Expiratory Volume; D005787:Gene Frequency; D020022:Genetic Predisposition to Disease; D005838:Genotype; D006801:Humans; D015227:Lipid Peroxidation / Q000235:genetics; D008297:Male; D018384:Oxidative Stress / Q000235:genetics; D010366:Peak Expiratory Flow Rate; D020641:Polymorphism, Single Nucleotide; D011401:Promoter Regions, Genetic / Q000235:genetics*; D018154:Slovakia / Q000453:epidemiology; D013438:Sulfhydryl Compounds / Q000097:blood; D017392:Thiobarbituric Acid Reactive Substances / Q000032:analysis
chemical_list: D001798:Blood Proteins; D013438:Sulfhydryl Compounds; D017392:Thiobarbituric Acid Reactive Substances; C577219:CAT protein, human; D002374:Catalase
keywords: Asma bronquial; Bronchial asthma; Catalasa; Catalase; Children; Gene polymorphism; Lesión oxidativa; Niños; Oxidative damage; Polimorfismo genético