Vitamin B12 is involved in biochemical metabolic pathways. B12 deficiency is common in childhood when the need for the vitamin increases and growth and development occur. Various hematological, neurological, psychiatric, and gastrointestinal disorders are observed in its deficiency. In addition, B12 deficiency is associated with oxidative stress and DNA damage. Therefore, the aim of our study is to evaluate oxidative stress, thiol/disulfide homeostasis, and DNA damage pre and post-treatment in children diagnosed with B12 deficiency. A total of 40 children with B12 deficiency were included in the study after the consent form was approved. Blood was drawn from children pre and posttreatment. Hemoglobin (HGB), hematocrit (HCT), and red blood cells (RBC) were measured by autoanalyzer; total antioxidant status (TAS), total oxidant status (TOS), total thiol (TT), and native thiol (NT) were measured by the photometric method, and DNA damage was analyzed by the comet assay method. Oxidative stress index (OSI) and disulfide (DIS) values were calculated. As a result of the experiments, HGB, HCT, and RBC increased with treatment. While TAS, TT, and NT as antioxidant parameters increased; TOS, OSI, and DIS decreased with treatment compared to pretreatment. DNA damage was also found to decrease with treatment. Additionally, these data were statistically significant (p < 0.001). It was found that oxidative stress and DNA damage decreased with oral B12 treatment in children with B12 deficiency, and clinical parameters were also improved.
Keywords: B12; DNA damage; cobalamin; deficiency; oxidative stress.