The Association of Oxidative and Antioxidant Potential with Cardiometabolic Risk Profile in the Group of 60- to 65-Year-Old Seniors from Central Poland

Abstract

Pathogenesis of cardiovascular diseases is caused by, inter alia, oxidative stress. On the other hand, cardiovascular risk factors may cause redox imbalance. The pathological pathways between those components are to be determined. In the group comprised of 300 sex-matched subjects, we evaluated a number of cardiovascular risk factors: blood pressure, body mass, lipids, glucose, homocysteine, uric acid, von Willebrand factor (vWF), VCAM-1 and ICAM-1. The presence of cardiovascular diseases and drugs for their treatment were examined. Secondly, we assessed total antioxidative status (TAS), total oxidative status (TOS) and other markers of oxidative stress. TAS was inversely related to LDL cholesterol. TOS was positively associated with BMI and female sex, but negatively associated with the use of angiotensin II receptor antagonists. Plasma lipid peroxides concentration was positively related to ICAM-1 and presence of stroke, whereas platelet lipid peroxides were positively associated with vWF. Platelets proteins thiol groups were in a positive relationship with vWF, but in a negative relationship with uric acid and diagnosed lipid disorders. Both free thiol and amino groups were positively associated with plasma glucose. Platelets free amino groups were related to platelets count. Superoxide generation by blood platelets (both with and without homocysteine) was positively connected to glucose level. Among women, oxidative markers appear to be more related to glucose level, whereas among men they are related to body mass indices. TAS, TOS and oxidative markers are largely related to modifiable cardiovascular risk factors such as body mass, and intake of drugs such as angiotensin II receptor blockers. Plasma and platelet oxidation markers appear to be especially associated with glucose concentration. The presented analyses unanimously indicate strong connections between cardiovascular risk factors and redox potential and specify how cardiometabolic interventions may counter-balance oxidative stress.