[ON THE PLURALITY OF THE WAYS OF RADIATION ADAPTIVE RESPONSE FORMATION IN HUMAN PERIPHERAL BLOOD LYMPHOCYTES].
The current review summarizes the results of investigations on the phenomenon of the decrease of cell radiosensitivity after the impact of various damaging factors in small doses. This phenomenon is known as an adaptive response (AR). It has been described in a number of biological objects, but the author has reviewed only the researches that have been done on human peripheral blood lymphocytes. Lymphocyte AR is specifically characterized by the fact that the entire cascade of events that decrease radiosensitivity occurs during one mitotic cycle. This feature distinguishes lymphocyte AR from the phenomenon of cell adaptation to chronic small dose irradiation. In this review, the author pays special attention to research on the initial stages of the AR formation. The author presumes that the AR occurs as a result of nonspecific intracellular changes that are a signal of the disruption in cell homeostasis. Several researchers define the state that results from this as the state of stress. After a cell transfers to this state there is a launch of biochemical processes that are able to protect the cell in case of future exposure to large doses of damaging factors (including irradiation). These processes are not determined strictly by the initial stimulus and are not initiated directly by the impact of the external factor that induced the AR. The particular method of decreasing radiosensitivity has not been determined and its selection depends on cell genotype, conditions of the experiment, etc. This might be the synthesis of various types of reparation enzymes, the synthesis of antioxidant enzymes, the activation of cell division or apoptosis. Cells that do not turn into the stress state do not form an AR. If there is no damaging shock-like impact after the cell enters the stress, the cell gets back to the normal rest state and the ability to form an AR disappears.
A M
AM
Serebryanyi
D000222:Adaptation, Physiological / Q000235:genetics*; D018797:Cell Cycle Proteins / Q000235:genetics / Q000378:metabolism; D004249:DNA Damage; D004260:DNA Repair; D005786:Gene Expression Regulation; D005838:Genotype; D006706:Homeostasis; D006801:Humans; D007963:Leukocytes, Mononuclear / Q000166:cytology / Q000378:metabolism / Q000528:radiation effects*; D008938:Mitosis; D011836:Radiation Tolerance / Q000235:genetics*; D011839:Radiation, Ionizing; D015398:Signal Transduction; D013312:Stress, Physiological
D018797:Cell Cycle Proteins