[Mechanisms of cerebral radiation syndrome].
Postradiation DNA breaks activate the repair enzyme, Adenosine diphosphoribosil transferase, which consumes NAD as a substrate and causes neuronal NAD and then ATP pool depletion; here this is considered to be the crucial links of the cerebral radiation syndrome (CRS) mechanism. Two ways of its metabolic correction were examined: (a) prevention of postradiation NAD depletion by administration of the enzyme inhibitor and (b) shunting NAD-dependent oxidative phosphorilation path of ATP resynthesis by administration of substrate of NAD-independent oxidation.
Military-Medical Academy, St. Petersburg, 194175 Russia.
Iu Iu
IuIu
Ivnitskiĭ
A V
AV
Nosov
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Malakhovskiĭ
D000818:Animals; D001921:Brain / Q000201:enzymology* / Q000528:radiation effects*; D008297:Male; D009243:NAD / Q000378:metabolism*; D010085:Oxidative Phosphorylation; D011833:Radiation Injuries, Experimental / Q000201:enzymology* / Q000503:physiopathology; D051381:Rats; D017208:Rats, Wistar; D013577:Syndrome
D009243:NAD