INCREASED OXIDATIVE STRESS AND CHANGES IN THE LEVEL OF EXPRESSION OF THE BCL AND BAX GENES IN CHILDREN WITH SEVERE ASD

Autism Spectrum Disorders (ASDs) are a heterogeneous group of psychiatric disorders most commonly seen in children. Patients with ASD are characterized by cognitive, behavioral, communicative deficits and obsessive stereotypical behavior. At that moment, the etiology and pathogenesis of ASD is one of the most important problems in child psychiatry. Patients with ASD are characterized by increased oxidative stress. The aim of this study was to characterize the role of oxidative stress in patients with ASD in enhancing the level of apoptosis. The clinical group consisted of 133 children with ASD (DSM-5), 4-12 years old, who were followed up by the Federal State Budget Scientific Institution National Center for Health Care. Children with ASD were divided into two subgroups according to the severity of the course of the disease, according to CARS scores. The control group included 27 healthy children. Lymphocytes were isolated from whole blood by centrifugation in a ficoll-urographin gradient. The level of gene expression in peripheral blood lymphocytes of patients with ASD and healthy controls was assessed by quantitative determination of the mRNA level by real-time PCR and by the level of protein in cells, flow cytometry. cytofluorometry. In the lymphocytes of children from the subgroup with mild and moderate forms of ASD, the level of ROS was increased, but the level of significance was not reached, while in the lymphocytes of children with severe ASD, the level of ROS was 2.2-2.5 times higher than in children of the control group. groups (p<0.01). The level of expression of the anti-apoptotic gene BCL2 in lymphocytes of children with severe ASD was reduced by 2-2.5 times (p<0.01), and the level of expression of the pro-apoptotic BAX gene was increased by 1.8-2.3 (p<0.01) times higher compared to the control. This may indicate an increase in oxidative stress and apoptosis in patients with severe ASD.