[Mechanisms of genome instability in children with periventricular leucomalacia that resulted in cerebral palsy].

The activity of free-radical oxidation and the level of genome instability in children with periventricular leucomalacia that resulted in cerebral palsy have been studied. Genome destabilization, i.e., the elevation of erythrocyte micronuclei in the peripheral blood, has been reported. There was a correlation of a number of cells with cytogenetic rearrangements with the activity of antioxidant defense enzymes and the malonaldehyde level. It has been shown that genome instability occurs during the activation of endogenous mutagenesis and reduction of antiradical and antimutagenic defense. Having, along with the neurotrophic effect, antiradical and antimutagenic effects, cortexin is capable to inhibit the pronounced processes of free-radical oxidation and endogenous mutagenesis in patients with periventricular leucomalacia that resulted in spastic dyplegia exerting.