[Prevention of structural damage to myocardial DNA caused by emotionally painful stress by means of beta-adrenoreceptor and lipid peroxidation blockade].

Emotional-painful stress was accompanied by an increase in the rates of depolymerization and of repairatory replication of heart muscle DNA. When the repairatory replication of DNA was repressed by actinomycin D, the rate of its depolymerization was simultaneously increased. A beta-adrenoreceptor blocking agent inderal and an inhibitor of lipoperoxidation ionol prevented the DNA depolymerization and activation of the polymer synthesis under the stressory conditions. These data corroborate the hypothesis that stress favors an increase in content of catecholamines, increasing the rate of lipoperoxidation and producing free radicals responsible for impairment of heart muscle DNA. In ontogenesis the multiple damage-repair cycles in DNA apparently lead to accumulation of genetic errors, which may be among the reasons of senescense.