[Elimination of stress-induced activation of DNA reparative synthesis in the myocardium by increasing the load on the heart].
The rate of DNA reparative synthesis was studied in the nucleus of myocardial cells in the heart compensatory hyperfunction (HCH) induced by the aorta coarctation and in animals exposed to surgical stress without the aorta coarctation. It was established that both surgery and emotional painful stress activated the DNA reparative synthesis in myocardial cells. For example, 12-24 hrs following the surgery the DNA reparation rate exceeded control values by 50-74%. HCH induced no changes in the DNA reparation rate in nuclei of myocardial cells. The mechanism of stress-induced DNA damage is discussed and a hypothesis is put forward on stabilizing the effect of hyperfunction on the DNA structure.
Meerson
F Z
FZ
Iavich
M P
MP
Rozhitskaia
I I
II
Golubeva
L Iu
LIu
D000818:Animals; D001017:Aortic Coarctation / Q000503:physiopathology; D002467:Cell Nucleus / Q000187:drug effects / Q000378:metabolism; D004247:DNA / Q000096:biosynthesis* / Q000187:drug effects; D004260:DNA Repair / Q000187:drug effects; D006321:Heart / Q000187:drug effects / Q000503:physiopathology*; D006918:Hydroxyurea / Q000494:pharmacology; D008297:Male; D009206:Myocardium / Q000378:metabolism*; D051381:Rats; D013312:Stress, Physiological / Q000503:physiopathology*; D013315:Stress, Psychological / Q000503:physiopathology*; D014316:Tritium
D014316:Tritium; D004247:DNA; D006918:Hydroxyurea
Ustranenie stressornoĭ aktivatsii reparativnogo sinteza DNK v miokarde posredstvom uvelicheniia nagruzki na serdtse.