[The antimutagenic action of a preparation of a species-nonspecific interferon].
The human gene-engineering gamma-interferon agent gammaferon (GF) is demonstrated to lower the level of chromosomal aberrations and release of cyclophosphamide-induced micronuclei in murine bone marrow cells. A model is suggested for regulating the ratio of single to multiple chromosomal aberrations induced by cyclophosphamide by altering the antioxidative status of the body. With this model, it was shown that the antimutagenic effects of GF were caused by two factors: the antioxidative effect of the corresponding placebo and the unknown (but none antioxidative) effect of gamma-interferon itself. Erythrocytic resistance to in vitro oxidative disturbance in the Fe2+/system was used as an integral measure of the body's antioxidative status.
Ingel'
F I
FI
Sakharova
T A
TA
Khripach
L V
LV
Revazova
Iu A
IuA
D000818:Animals; D016587:Antimutagenic Agents / Q000494:pharmacology*; D001205:Ascorbic Acid / Q000494:pharmacology; D001853:Bone Marrow / Q000187:drug effects; D001854:Bone Marrow Cells; D016009:Chi-Square Distribution; D002869:Chromosome Aberrations; D003520:Cyclophosphamide / Q000494:pharmacology; D006461:Hemolysis / Q000187:drug effects; D007371:Interferon-gamma / Q000494:pharmacology*; D051379:Mice; D008810:Mice, Inbred C57BL; D008808:Mice, Inbred CBA; D011994:Recombinant Proteins; D013045:Species Specificity
D016587:Antimutagenic Agents; D011994:Recombinant Proteins; D007371:Interferon-gamma; D003520:Cyclophosphamide; D001205:Ascorbic Acid