Association of Peripheral Markers of Oxidative Stress with Clinical Parameters and Inflammatory Factors in Alcoholic Patients.

Abstract

One of the fundamental problems in studying addiction is elucidation of mechanisms of alcohol dependence (AD) development. Disturbances of cellular redox balance and inflammation play an important role in AD pathogenesis. Deciphering associations between biological and clinical indicators can elucidate molecular mechanisms of disease pathogenesis. The aim of the work was to study peripheral markers of oxidative stress in patients with AD during early abstinence period and to identify their relationship with clinical parameters of the disease and inflammatory factors. In total, 84 patients with AD were studied (average age, 44.3 ± 8.2 years). The analyzed clinical parameters included patient's age, age of alcohol withdrawal syndrome (AWS) formation, disease duration, and AWS duration. The markers of oxidative stress determined in the blood plasma were oxidation products of proteins (protein carbonyls, PCs), lipids (thiobarbituric acid-reactive products, TBA-RPs), and DNA (8-hydroxy-2'-deoxyguanosine, 8-OH-dG). The content of inflammatory mediators, such as proinflammatory cytokines (IFNγ, IL-1β, IL-6, IL-8, IL-17A, TNFα) was determined in the blood serum. Blood samples of 80 conditionally healthy men (average age, 40.9 ± 9.6 years) were used as a control. Patients with AD demonstrated an increase in the content of PCs, TBA-RPs, and all analyzed cytokines (but not 8-OH-dG) compared to the control individuals. There was a direct correlation between the TBA-RP content and disease duration and inverse correlation of the PC content with the age of AWS formation and AWS duration. The content of PCs demonstrated an inverse correlation with the IL-6 concentration in the blood plasma. We also observed a positive correlation between 8-OH-dG and IL-6, TBA-RPs and IL-8, and TBA-RPs and TNFα. Therefore, the early abstinence period in patients with AD was characterized by a pronounced oxidative stress and inflammation. The obtained results expand the knowledge on the integrative contribution of oxidative stress and inflammatory factors to the AD pathogenesis and can be used in the development of new therapies.