ESPE Abstracts

Introduction: Increased cytokine release, impaired antioxidation and reactive oxygen species (ROS) have been shown in β-cells in pathogenesis of T1DM. Increased ROS leads to formation of covalent bonds between the sulfur atoms, leading to disulphide conversion. Displacement to disulphide form of this thiol/disulphide balance starts the oxidative damage. This study evaluates the thiol/disulphide balance in children with T1DM.

Material and method: Thiol/disulphide balance evaluated in 30 patients with T1DM and 30 healthy volunteer children. Total thiol, native thiol and disulphide levels studied by Erel & Neselioglu’s newly developed automatic measurement method.

Results: There was no difference in age and gender of T1DM group (17 f/ 13 m, mean age:11.75±2.71 years) and control group (12 f/ 18 m; mean age:11.54±2.55 years). In T1DM group, results were as; native thiol: 388.3±76.7 μmol/l, total thiol: 426.2±87 μmol/l, disulphide: 18.9±7 μmol/l, in control group, were as; native thiol: 423.1±45.2 μmol/l, total thiol: 455.7±49.9 μmol/l, disulphide: 16.2±5.6 μmol/l. Disulphide/native thiol, disulphide/total thiol ratios were significantly higher in the type 1 diabetes mellitus group (P:0.005, P:0.004), but native thiol levels, native thiol/total thiol ratio were significantly lower than the control group (P:0.036, P:0.015). There was no statistically significant correlation between demographic data and thiol/disulphide subgroups.

Discussion: This is the first study demonstrating that dynamic thiol/disulphide homeostasis in children with T1DM shifts to the disulphide direction. It is suggested that this shift is caused by oxidative damage of β cells. New studies about thiol/disulphide homeostasis in children with T1DM can lead to early detection of oxidative damage of β cells.