Genetic Variants in the Manganese Superoxide Dismutase 2 Gene and in the Catalase Gene are not Associated With Alcoholic Chronic Pancreatitis. (26th June 2017)

• Record Type: Journal Article
• Authors: Schneider, Alexander; Rosendahl, Jonas; Bugert, Peter; Weiss, Christel; Unterschütz, Heike; Kylanpää-Bäck, Marja-Leena; Lempinen, Marko; Kemppainen, Esko; Diaconu, Brindusa L.; Ebert, Matthias P.; Pfützer, Roland H.
• Is Part Of: Alcohol and alcoholism. Volume 52:Number 5(2017)
• Page Start: 535
• Page End: 541
• Publication Date: 2017-06-26
• Subjects: Alcoholism -- Periodicals; 616.861005
• DOI: 10.1093/alcalc/agx039
• Languages: English
• ISSNs: 0735-0414

Abstract

Abstract: Aims: Oxidative stress may contribute to the development of chronic pancreatitis (CP). The enzymes manganese superoxide dismutase 2 (MnSOD, SOD2) and catalase (CAT) counteract free radical activity within the mitochondria and the cytosol. Moreover, CAT activity contributes to the transformation of ethanol to acetaldehyde, a toxic intermediate product of ethanol metabolism, which has been associated with pancreatic damage. Common functional polymorphisms have been described in the MnSOD gene [rs4880, NM_000636.3:c.47 T > C, alanine (ALA) to valine (Val)] and in the CAT promoter region [rs1001179, NG_013339.1:g.4760 C > T]. We investigated whether these polymorphisms are associated with alcoholic CP. Methods: We genotyped 470 patients with alcoholic CP for these MnSOD and CAT polymorphisms. We also analysed these variants in 357 healthy control subjects, and in an additional control group of 113 individuals with non-alcoholic CP. We used the age at onset of CP as marker of disease severity and investigated whether different genotypes are associated with different ages at onset. In patients with alcoholic CP, we investigated whether an interaction exists between smoking behaviour and genotypes by comparing genotype distributions in smokers and non-smokers. Results: We did not observe significant differences of genotype frequencies between patient groups and controls. In patient groups, we did not find significant differences in the ages at onset between different genotypes. We did not observe an interaction between these polymorphisms. We did not find an association of these variants with smoking behaviour. Conclusions: The investigated MnSOD and CAT polymorphisms do not predispose to the development of alcoholic CP. Short summary: Patients with alcoholic pancreatitis and controls were genotyped for polymorphisms in oxidative stress genes. There were no significant differences of genotype frequencies between patients and controls, and no association with the age at onset of disease was observed. The polymorphisms are not associated with the development of alcoholic pancreatitis.