En subjects were investigated in this study in order to evaluate the association of the MnSOD Ala16Val and GPx1 Pro198Leu polymorphisms with the coronary heart disease (CHD). Characteristics of the enrolled subjects stratified according to MnSOD and GPx1 polymorphisms are illustrated in Table 1. Results observation showed a significant difference between MnSOD genotype classes associated with male gender and diabetes mellitus. Whereas, a significant difference between GPx1 genotype groups was noted only according to LDL level in the study population. Biochemical examination of our population was carried out by testing several parameters (Table 1). Results showed a significant difference between genotype groups for antioxidant status. Indeed, SOD2 but not GPx1 activity decreased significantly in the presence of the mutated allele (Val and Leu, respectively). The same is true for total antioxidant status (TAS). In fact, significant reduced levels of TAS were detected in variant carrier groups. For other parameters, no differences were noted by genotype. In the whole population, genotype distribution of the Mn-SOD Ala16Val (CC/CT/TT: 92/172/103, 2 = 1.40, p = 0.24) and GPx1 Pro198Leu (CC/CT/TT: 180/152/35, 2 = 0.13, p = 0.72) variants satisfied the Hardy einberg equilibrium (p > 0.05) with a C allele frequency of 48.50 and 69.75 respectively for MnSOD and GPx1 genes (Table 1). Thonzonium (bromide) web Relationship between gene polymorphisms and CHD, as well as CHD risk estimation, were assessed by comparing Mn-SOD Ala16Val and GPx1 Pro198Leu genotype distribution among cases and controls (Tables 2, 3). Taking into account the significant difference detected between Mn-SOD genotype groups associated to some risk factors (Table 1), genotype distribution in control and case groups was studied by gender (Table 2). Several compounds proposed to act as antioxidants (AOX) in vivo [27] were considered in our study. We found a significant decrease in direct and total bilirubin in both male and female cases. Moreover, a significant difference at iron level was observed between controls and cases in the male group. However, in female group, an increase of uric acid was noted. No significant difference at albumin level was observed between cases and controls of male and female groups. SOD activity and TAS were measured in both control and CHD groups. In harmony with the first results obtained in the whole population after genotypeSouiden et al. Biol Res (2016) 49:Page 5 ofTable 1 Basic characteristics of the study population by genotypeTrait SOD genotype Ala/Ala (CC) (N = 92) Age (years) Body mass index (kg/m2) Male, n ( ) Hypertension, n ( ) Hyperlipidemia, n ( ) Diabetes mellitus, n ( ) Current Smokers, n ( ) Plasma glucose (mmol/l) LDL cholesterol (mmol/l) Triglycerides (mmol/l) HDL cholesterol (mmol/l) CRP (mg/l) Uric Acid ( ol/l) Total bilirubin ( ol/l) Direct bilirubin ( ol/l) Albumin (g/l) Iron ( ol/l) PubMed ID:https://www.ncbi.nlm.nih.gov/pubmed/25962748 SOD activity (U/gHb) GPx activity (U/gHb) TAS (mmol/l) 60.47 ?10.88 61 (66.30 ) 22 (23.91 ) 16 (17.39 ) 14 (15.22 ) 47 (51.08 ) 5.71 ?3.68 2.52 ?1.09 1.57 ?0.66 1.32 ?0.72 1.50 ?0.34 Ala/Val (CT) (N = 172) 62.42 ?11.98 88 (51.16 ) 43 (25.0 ) 27 (15.70 ) 20 (11.62 ) 86 (50.0 ) 5.25 ?2.26 2.46 ?1.02 1.63 ?0.70 1.45 ?0.74 1.61 ?0.44 313.69 ?108.9 13.32 ?6.52 5.91 ?2.09 43.06 ?4.47 17.34 ?5.37 1285.3 ?188.9 ?1.53 ?0.31 Val/Val (TT) (N = 103) 61.51 ?11.99 67 (65.05 ) 31 (30.10 ) 29 (28.15 ) 25 (24.27 ) 49 (47.57 ) 5.62 ?2.15 2.48 ?1.08 1.66 ?0.