title: [Acute radiation cerebral disorders as an effect of neuronal DNA damage].
abstract: Early transient incapacity and cerebral radiation syndrome were shown to result from the de-energizing of the brain due to NAD and ATP neuron pools depletion since DNA breaks stimulate the repair enzyme, ADP-ribosyltransferase, that consumes NAD as a substrate. The phenomenology of syndromes, peculiarities of the CNS repair and neutron RBE might be attributed to this mechanism. DNA is thus a common target for stochastic, deterministic and physiological effects of radiation.
authors.forename: V N
authors.initials: VN
authors.lastname: Malakhovskiĭ
mesh_terms: D000208:Acute Disease; D000818:Animals; D001921:Brain / Q000378:metabolism / Q000528:radiation effects*; D001927:Brain Diseases / Q000209:etiology* / Q000378:metabolism; D004247:DNA / Q000378:metabolism / Q000528:radiation effects*; D004249:DNA Damage; D004260:DNA Repair / Q000528:radiation effects; D009474:Neurons / Q000378:metabolism / Q000528:radiation effects*; D011833:Radiation Injuries, Experimental / Q000150:complications* / Q000378:metabolism
chemical_list: D004247:DNA
vernacular_title: Ostrye luchevye tserebral'nye narusheniia kak éffekt povrezhdeniia DNK neĭronov.