The antimutagenic effect of adaptation to stress

C57BL mice were adapted to moderate periodic hypoxia and repeated electric pain stresses of limited intensity. These animals adapted to each of the factors and control animals were given the potent mutagen, free radical oxidation activator dioxidine in a single dose of 300 mg/kg. Dioxidine administe...

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Bibliographic Details
Published inBiulleten' eksperimental'noi biologii i meditsiny Vol. 116; no. 9; p. 292
Main Authors Meerson, F Z, Kulakova, A V, Saltykova, V A
Format Journal Article
LanguageRussian
Published Russia (Federation) 01.09.1993
Subjects
Adaptation, Physiological - drug effects
Adaptation, Physiological - genetics
Animals
Bone Marrow - drug effects
Bone Marrow Cells
Chromosome Aberrations - genetics
Chromosome Aberrations - physiology
Hematopoietic Stem Cells - drug effects
Hypoxia - genetics
Hypoxia - physiopathology
Male
Mice
Mice, Inbred C57BL
Mutagenesis - drug effects
Mutagenesis - physiology
Mutagens - pharmacology
Pain - genetics
Pain - physiopathology
Periodicity
Quinoxalines - pharmacology
Stress, Physiological - genetics
Stress, Physiological - physiopathology
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Summary:C57BL mice were adapted to moderate periodic hypoxia and repeated electric pain stresses of limited intensity. These animals adapted to each of the factors and control animals were given the potent mutagen, free radical oxidation activator dioxidine in a single dose of 300 mg/kg. Dioxidine administered to unadapted animals resulted in chromosomal aberrations in 11% of stem bone marrow cells mainly due to the appearance of single and multiple chromosomes. Preadaptation to stress decreased the number of these dioxidine-induced chromosomal aberrations nearly twice. Adaptation to periodic hypoxia had no defensive action. As previously shown, adaptation to repeated stresses leads to the accumulation of heat-shock proteins (HSP) in the cellular nuclei of animals and prevents the degradation of isolated nuclei when single-chain DNA is added. Adaptation to hypoxia does not cause nuclear accumulation of HSP or prevents their degradation when unicellular DNA is supplemented. This suggests that the antimutagenic effect of stress adaptation is likely to be accounted for by the stabilizing action of HSP.
ISSN:0365-9615