Dynamic thiol/disulphide homeostasis as a novel indicator of oxidative stress in obese children and its relationship with inflammatory-cardiovascular markers

Objective: Childhood obesity is an important cause of cardiovascular risk with chronic inflammation. Oxidative stress may contribute to the pathogenesis of obesity-related cardiovascular pathologies. We aimed to evaluate thiol/disulphide homeostasis as a novel and sensitive marker of oxidative stress and to evaluate its relationship with some inflammatory and cardiovascular markers in obese children.
Methods: In this case-controlled study, 65 children with exogenous obesity and 64 healthy children, as a control group, were included. In both groups, thiol/disulphide homeostasis parameters and inflammatory (white blood cells, platelets, mean corpuscular volume, neutrophil/lymphocyte ratio, and high-sensitivity C-reactive protein) and cardiovascular (epicardial adipose tissue thickness and left ventricular mass index) markers were studied. Correlation analyses of thiol/disulphide homeostasis parameters with body mass index standard deviation scores (BMI SDS) and inflammatory and cardiovascular markers were performed. Receiver-operating characteristic analysis was performed to determine the sensitivity, specificity, and optimal cut-off values of thiol/disulphide homeostasis parameters.
Results: Native thiol, total thiol, and native thiol/total thiol ratios (antioxidant parameters) were lower (p<0.05) and disulphide/native thiol and disulphide/total thiol ratios (oxidant parameters) were higher in the obese group than in the control group (p<0.01). A positive correlation of oxidant parameters with BMI SDS and inflammatory markers was found. However, a negative correlation of antioxidant parameters with BMI SDS and inflammatory markers was found. The specificities of disulphide/native thiol and disulphide/total thiol ratios were higher in the obese group.
Conclusion: The impairment in thiol/disulphide homeostasis, which is indicative of oxidative stress, is associated with inflammation in obesity. In addition, cardiovascular involvement may also contribute to this impairment.