title: Correlation of EPHX1, GSTP1, GSTM1, and GSTT1 genetic polymorphisms with antioxidative stress markers in chronic obstructive pulmonary disease.
abstract: This study was undertaken to ascertain if a relationship existed between oxidative status and polymorphisms of microsomal epoxide hydrolase X1 (EPHX1), glutathione S-transferase P1 (GSTP1), GSTM1, and GSTT1 in chronic obstructive pulmonary disease (COPD). Erythrocyte glutathione peroxidase (GSH-px), glutathione reductase (GR), superoxide dismutase (SOD), catalase (CAT), and plasma GST activities and total antioxidant status (TAS) as antioxidative stress markers were determined and compared either with individual and combined genotypes of EPHX1 exon 3, GSTP1 exon 5, GSTM1, and GSTT1 polymorphisms in COPD patients and healthy controls from the central area of Tunisia. Statistical data processing revealed significantly lower GSH-px, GR, SOD, CAT, GST, and TAS values in COPD patients in comparison to the control group (P < .001). As for genotypes, there was a no significant association in each of the 6 parameters and individual genotypes (P > .05). A significant correlation between the studied parameters and combined null GSTM1/null GSTT1 (GSH-px: P < .001, GR: P = .026, CAT: P = .018, GST: P = .022, TAS: P = .046), His113His EPHX1/null GSTM1 (GSH-px: P = .001, GST: P = .0012, TAS: P = .013), His113His EPHX1/Val105Val GSTP1 (GSH-px: P = .048, CAT: P = .026, GST: P = .031), and null GSTM1/Val105Val GSTP1 (GSH-px: P = .011, GR: P = .0028, GST: P = .0054, TAS: P = .032) was found in patients. In conclusion, combined genetic polymorphisms of GSTM1, GSTT1, GSTP1, and EPHX1 may have favorable effects on redox balance in COPD patients.
authors.affiliation: Biochemistry and Molecular Biology Laboratory, Faculty of Pharmacy, Monastir, Tunisia. lakhdarramzi@yahoo.fr
authors.forename: Ramzi
authors.initials: R
authors.lastname: Lakhdar
authors.forename: Sabri
authors.initials: S
authors.lastname: Denden
authors.forename: Manel Haj
authors.initials: MH
authors.lastname: Mouhamed
authors.forename: Abdelkader
authors.initials: A
authors.lastname: Chalgoum
authors.forename: Nadia
authors.initials: N
authors.lastname: Leban
authors.forename: Jalel
authors.initials: J
authors.lastname: Knani
authors.forename: Gérard
authors.initials: G
authors.lastname: Lefranc
authors.forename: Abelhadi
authors.initials: A
authors.lastname: Miled
authors.forename: Jemni
authors.initials: J
authors.lastname: Ben Chibani
authors.forename: Amel Haj
authors.initials: AH
authors.lastname: Khelil
mesh_terms: D015415:Biomarkers / Q000032:analysis; D016022:Case-Control Studies; D004851:Epoxide Hydrolases / Q000235:genetics*; D051549:Glutathione S-Transferase pi / Q000235:genetics; D005982:Glutathione Transferase / Q000235:genetics*; D006801:Humans; D010084:Oxidation-Reduction; D018384:Oxidative Stress / Q000235:genetics*; D011110:Polymorphism, Genetic; D029424:Pulmonary Disease, Chronic Obstructive / Q000235:genetics* / Q000378:metabolism
chemical_list: D015415:Biomarkers; D004851:Epoxide Hydrolases; D051549:Glutathione S-Transferase pi; D005982:Glutathione Transferase; C413545:glutathione S-transferase T1; C496556:GSTP1 protein, human; C522330:EPHX1 protein, human