Role of Cigarette Smoking on Serum Angiotensin-Converting Enzyme and Its Association With Inflammation and Lipid Peroxidation

Introduction Cigarette smoking promotes angiotensin-converting enzyme (ACE) production and causes a substantial change in inflammation and oxidative stress, resulting in an increase in antioxidant activity and lipid peroxidation. Objective The study's goal is to determine the role of cigarette smoking on serum ACE and its relation with inflammatory markers and lipid peroxidation. Methods The cross-sectional study consists of three groups. The study participants are all men between the age group of 20 to 55 years. Group 1 includes 120 healthy controls as nonsmokers, Group 2 consists of 120 active smokers with coronary heart disease (CHD) and Group 3 includes 120 active smokers with diabetic CHD patients attending the SRM Medical College Hospital in Tamil Nadu for cardiology and medical Outpatient. Measurements of serum ACE, oxidized low-density lipoprotein (oxLDL), high-sensitivity C-reactive protein (hsCRP), and matrix metalloprotease-9 (MMP-9) were performed using the ELISA method (enzyme-linked immunosorbent assay). Using a spectrophotometric approach, the total antioxidant capacity and lipid peroxidation, particularly Malondialdehyde (MDA), were assessed. Results The mean serum ACE (92.35±10.28), oxLDL (48.59±8.56), hs-CRP (5.87±1.62), MMP-9 (89.20±30.19), and MDA (1.146±0.198) levels were significantly (p-value <0.0001) higher in smokers with CHD and diabetes (group 3) when compared to group 1 and group 2. On the other hand, the total antioxidant capacity (0.413±0.097) of smokers of group 3 was found to be (p<0.0001) significantly lower than those of group 1 and group 2. The study also demonstrated a significant correlation between ACE with MDA, ox-LDL, total antioxidant capacity, hs-CRP, MMP-9, smoking load, and smoking intensity in smokers. Conclusion The study concludes a substantial correlation exists in smokers owing to ACE modification, which results in inflammation and lipid peroxidation activation. This is strongly associated with an increased risk of major cardiovascular events.