RESUMO
Disorders in the DNA repair in the human lymphocytes isolated from patients with Marfan's syndrome, homocystinuria, schizophrenia, and gout have been found. In this investigation criteria used estimating the DNA repair were the following: host cell reactivation (vaccinia virus reactivation) and its mutagenesis, DNA repair synthesis, resynthesis of DNA breakages. Lymphoblastoid interferon was used as a modulator of DNA repair activity. Pretreatment of normal human cells with interferon stimulated all steps of DNA repair. In human cells with disorders, interferon stimulated DNA repair (XP) in some cases but failed in others.
Assuntos
Reparo do DNA , DNA/biossíntese , Dano ao DNA , Reparo do DNA/efeitos dos fármacos , Reparo do DNA/genética , Reparo do DNA/efeitos da radiação , Gota/genética , Gota/metabolismo , Homocistinúria/genética , Homocistinúria/metabolismo , Humanos , Técnicas In Vitro , Interferon Tipo I/farmacologia , Linfócitos/efeitos dos fármacos , Linfócitos/metabolismo , Linfócitos/efeitos da radiação , Síndrome de Marfan/genética , Síndrome de Marfan/metabolismo , Mutagênicos/farmacologia , Esquizofrenia/genética , Esquizofrenia/metabolismo , Xeroderma Pigmentoso/genética , Xeroderma Pigmentoso/metabolismoRESUMO
Fibroblasts obtained from biopsied material and lymphocytes from patients with homocystinuria were studied for repair activity using the criterion of repair of DNA breaks induced by 4-nitroquinoline 1-oxide and gamma-irradiation and criteria of reactivation and induced mutagenesis of vaccinia virus. Lymphocytes showed defective DNA repair for all these criteria. In fibroblast cultures, the inhibition of cell-repair activity for the gamma-type was retained. The number of spontaneous and gamma-induced virus mutations increased as passaging of fibroblasts proceeded.
Assuntos
Dano ao DNA , Reparo do DNA , Homocistinúria/genética , 4-Nitroquinolina-1-Óxido , Células Cultivadas , Dano ao DNA/efeitos da radiação , Fibroblastos , Raios gama , Células HeLa , Humanos , Linfócitos/fisiologia , Vaccinia virus/genética , Replicação Viral , Xeroderma Pigmentoso/genéticaRESUMO
We studied the effect of cadmium chloride on: (1) the DNA of human cells; (2) the mutagenic effect of reproducing Kilham virus; (3) the synthesis of virus-induced interferon, and (4) the reproduction of oncogenic (mammalian leucosis) virus. Cadmium chloride caused degradation of DNA in human- and rat-embryo cells. Culture infected by the virus in the presence of cadmium sulphate had the highest yield of cells with chromosomal aberrations. Cadmium chloride caused marked inhibition of the virus-induced synthesis of interferon. The introduction of cadmium chloride into diploid cells infected by the leucosis virus caused a 3-4 fold increase in the yield of virus-induced transformation foci.
Assuntos
Cádmio/farmacologia , DNA/metabolismo , Interferons/biossíntese , Linhagem Celular , Cloretos/farmacologia , Aberrações Cromossômicas , Humanos , Mutação , Retroviridae/efeitos dos fármacos , Replicação ViralRESUMO
Evidence was obtained indicating differences in the survival rate of Western equine encephalomyelitis virus after exposure to ultraviolet radiation and methyl methanesulfonate in commercial and leukosisfree chick embryo cells that differed in repair activity. The levels of spontaneous mutagenesis (on the basis of the yield of small palque variants of the encephalomyelitis virus) did not essentially change when the virus was passage in leukosis-free chick embryo cells, whereas an increase in the number of small palque variants was observed in the cells of commercial chick embryos. A 10-fold increase in the number of induced virus variants was observed in commercial chick embryo cells in experiments with methyl methanesulfonate as compared with the contorl, whereas the induction of virus variants was not noted in leukosis-free cells.
