Biochemical Assessment of Hyperhomocysteinemia-Mediated Oxidative Stress in Coronary Artery Disease Patients: A Hospital-Based Cross-Sectional Study

This study aimed to assess the status of B-vitamins (folate, vitamin B6, and B12) and homocysteine (HCY) in the sera of Omani coronary artery disease (CAD) patients. Sixteen Omani patients (10 males and 6 females) gave consent for blood sampling and were enrolled in the study on voluntary basis. All patients were evaluated for their anthropometric and biochemical measurements of B-vitamins, glutathione (reduced and oxidized), HCY, and quantification of N-homocysteinylated albumin protein. It was observed that both male and female patients had a comparable age (57.64 ±9.86, 56.5 ±10.04 years, respectively) with no significant difference, P = 0.69 and both genders were obese based on their body mass index (31.22 ± 8.17 kg/m²for males and 30.26 ± 4.70 kg/m²for females). Serum levels of folate, vitamins B6, and B12 were lower than the normal reference values in all the study participants. There was depletion in glutathione levels (higher level of oxidized glutathione versus lower level of reduced glutathione) in the sera of all study participants. High serum HCY levels in both males and females (75.81±9.21 and 68.66±8.1 μmol/L, respectively) suggest that both males and females had hyperhomocysteinemia. Correlation coefficient analysis revealed that the serum HCY levels were negatively correlated with serum reduced glutathione, folic acid, vitamins B6, and B12 levels in both male and female study participants. The serum HCY level was positively correlated with age, body mass index, and serum oxidized glutathione. Proteomic measurements of N-homocysteinylation in serum albumin revealed that N-homocysteinylated albumin was present in all the assayed serum samples of study participants. The results suggest that low serum status of B-vitamins might act as a metabolic trigger for the observed hyperhomocysteinemia, oxidative stress, and pathological formation of N-homocysteinylated albumin protein, which collectively aggravates the CAD risk in the studied Omani patients.