Association Between Serum Paraoxonase-1 Activity and p53 Protein Levels in Smoking Patients with Hypertension

Abstract

Background: Smoking is a major driver of genetic instability and physiological alterations that escalate cardiovascular risk and cancer. Smoking a source of oxidative stress and a well-known risk factor for hypertension.
The Aim : to evaluate oxidative stress and DNA damage by quantifying 8-OHdG and TP53 levels, with the activity of the antioxidant enzyme PON-1, in smokers, and to examine the influence of hypertension and amlodipine treatment on these parameters.
Method: A total of 177 participant were recruited and divided into three groups: (1) hypertensive smokers group, (2) normotensive smokers group and (3) a control group. The ages of participants ranged between (26-64) years. Serum 8-OHdG ,TP53 levels were measured using ELISA technique, and the PON-1 activity were measure by using standard laboratory methods.
Results: Statistical analysis revealed a substantial elevation (p < 0.001) in 8-OHdG and TP53 levels among smokers relative to the control group. The group of smokers with hypertension exhibited the highest levels (140.60 ng/ml and 5534.2 pg/ml, respectively). PON-1 enzyme activity was markedly diminished in smokers, particularly in those with hypertension (4.07 kJ/L), compared to smokers with normal blood pressure (6.02 kJ/L) and healthy individuals (9.67 kJ/L).
Conclusion: Smoking causes severe depletion of the antioxidant defense system (PON-1) and increase gene damage (8-OHdG, TP53). Although patients were receiving amlodipine treatment, this treatment was insufficient to reverse the observed genetic damage and oxidative stress.