[Molecular and cellular mechanisms of late radiation injuries].
Late radiation damages arise more often in nonproliferating or slow proliferating tissues after local irradiation in large (intolerable) doses of ionizing radiation. Obviously the late radiation effects are induced by radiation damages to capillaries and disturbances of microcirculation in tissues. This is a basis for tissue hypoxia, "oxidative stress" and loss of parenchyma cells. The direct radiation effect on parenchyma cells has as a rule little importance for production of late radiation damages. Other type of late radiation damages can be discovered after sublethal irradiation of whole body. This is a cause of decrease of life span. In this case the important factors are also damages of vessels, disturbances in microcirculation and loss of parenchyma cells in "target" organs especially in neuroendocrine and immune systems. The new data on the possibility to decrease the late radiation damages after local or whole body irradiation using postradiation treatment with pulsed electric field (PEF) are considered. Mechanisms of PEF effects are explained in terms of its ability to induce nitric oxide production which causes intensification of blood microcirculation, as well as increase in SOD production and activity of repair enzymes.
Konopliannikov
A G
AG
Medical Radiological Research Center, Russian Academy of Medical Sciences, Obninsk.
D000818:Animals; D002455:Cell Division / Q000528:radiation effects; D015687:Cell Hypoxia; D006801:Humans; D008136:Longevity / Q000528:radiation effects; D008833:Microcirculation / Q000528:radiation effects; D009569:Nitric Oxide / Q000378:metabolism; D018384:Oxidative Stress / Q000528:radiation effects; D011832:Radiation Injuries / Q000378:metabolism* / Q000473:pathology; D013997:Time Factors
D009569:Nitric Oxide
Molekuliarnye i kletochnye mekhanizmy pozdnykh luchevykh povrezhdeniĭ.