Background. Magnesium (Mg), selinium (Se), zinc (Zn), manganese (Mn), and copper (cu) are involved in the mechanisms of antioxidant defense. Mn and cu, which participate in the generation of reactive oxygen species (ROS), also have pro-oxidative properties. Objectives. To evaluate the levels of Mg, Se, Zn, Mn, and cu, as well as the effectiveness of antioxidant defense mechanisms in children with Type 1Diabetes Mellitus (T1DM) and in their siblings. The preliminary findings were originally reported in 2009 at the 35 th annual conference of the International Society for Pediatric and adolescent Diabetes (ISPaD) in Ljubljana, Slovenia. Material and Methods. The study involved 87 children with T1DM, 2-19 years old, treated for T1DM for an average of 3.5 years. The sibling and control groups comprised 27 and 41 children, aged 4.5-16.5 years and 10.5-18 years respectively. The parameters named above were assessed in relation to metabolic compensation levels (Hb a1c ) and disease duration. Results. compared with the control group, T1DM children had lower plasma levels of Mg and Zn and higher levels of cu; the siblings had lower levels of Zn; T1DM children had lower copper/zinc superoxide dismutase (cuZnSOD) activity; and both T1DM children and their siblings had higher catalase (caT) activity and lower total antioxidant status (TaS) levels. Conclusions. There may be a correlation between impaired antioxidant status and Mg and Zn deficiency and increased cu levels in T1DM children. Oxidative stress in T1DM is accompanied by alterations in enzymatic activity and non-enzymatic mechanisms of antioxidant defense. The decreased TaS levels noted in T1DM patients may impair the effectiveness of non-enzymatic antioxidant systems. The increased caT activity and unimpaired selenium-dependent glutathione peroxidase (Se-GSHPx) activity point indirectly to enhanced ROS generation in T1DM children. The impaired antioxidant defense found in the siblings of T1DM patients may indicate that genetic factors play a role (Adv Clin Exp Med 2014, 23, 2, 259-268).