Heterogeneous distribution of DNA alkylation products in rat liver chromatin after in vivo administration of N,N-DI[14C]methylnitrosamine

Cooper, Helen K.; Margison, Geoffrey P.; O’Connor, Peter J.; Itzhaki, Ruth F.

doi:10.1016/0009-2797(75)90024-1

Cited by 29 publications

(2 citation statements)

References 29 publications

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“…Craddock (1973) has demonstrated that the half-life of m3A was 7 h in regenerating liver compared to 3 h in nonregenerating liver. In addition, since the sites of carcinogen interaction with DNA are nonrandomly distributed in DNA and the rates of removal of DNA-bound carcinogen from different regions of DNA are not the same (Cooper et al, 1975;Ramanathan et al, 1976a,b;Moyer et al, 1977;Metzger et al, 1977;Sarma et al, 1978;Schwartz & Goodman, 1979), and since only 21% of the liver DNA was anaylzed (see Table I), it is possible that the methylated bases characterized in the present study may constitute a selective distribution in certain segments of DNA that can be fractionated as hybrid DNA.…”

Section: Resultsmentioning

confidence: 99%

In vivo replication of hepatic deoxyribonucleic acid of rats treated with dimethylnitrosamine: presence of dimethylnitrosamine-induced O6-methylguanine, N7-methylguanine, and N3-methyladenine in the replicated hybrid deoxyribonucleic acid

Abanobi¹,

Columbano²,

Mulivor³

et al. 1980

Biochemistry

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Experiments were designed to determine whether some chemical lesions such as O6-methylguanine, N7-methylguanine, and N3-methyladenine induced in rat liver DNA by the hepatocarcinogen dimethylnitrosamine permit replication in vivo. For this purpose, [14C]dimethylnitrosamine was administered to methylate the parental strand of liver DNA. Four hours later, a time period when the carcinogen cannot be detected in either the liver or the blood, rats were subjected to partial hepatectomy in order to induce DNA replication. During the S phase, 5-bromo-2-deoxyuridine was administered to render the newly made strands heavy. The rebanded, hybrid, hepatic DNA of density 1.714 g/cm3 and greater was pooled from the neutral cesium chloride gradient, dialyzed, and lyophilized. The hybrid DNA was then treated with S1 nuclease to digest any single-stranded regions. The results obtained indicated the presence of O6-methylguanine, N7-methylguanine, and N3-methyladenine in S1 nuclease resistant, hybrid DNA. The results are interpreted to indicate that these chemical lesions permitted in vivo DNA replication.

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Section: Resultsmentioning

confidence: 99%

In vivo replication of hepatic deoxyribonucleic acid of rats treated with dimethylnitrosamine: presence of dimethylnitrosamine-induced O6-methylguanine, N7-methylguanine, and N3-methyladenine in the replicated hybrid deoxyribonucleic acid

Abanobi¹,

Columbano²,

Mulivor³

et al. 1980

Biochemistry

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“…Although it has been widely appreciated that mammalian cells repair radiation and chemical damage to DNA (4,5), recent advances in the understanding of chromatin structure (6,7) have focused attention on the importance of examining the role of chromatin structure in the repair process. In fact, work from several laboratories (8)(9)(10)(11)(12)(13)(14), including our own (15)(16)(17), has emphasized that an analysis of chromatin structure is crucial for understanding DNA damage and repair.…”

Section: Introductionmentioning

confidence: 99%

The distribution of DNA repair synthesis in chromatin and its rearrangement following damage with N-acetoxy-2-acetylaminofluorene

Tlsty

Lieberman

1978

Nucl Acids Res

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The distribution of DNA repair synthesis in the chromatin of confluent human diploid fibroblasts damaged with N-acetoxy-2-acetylaminofluorene has been studied. Kinetic analysis of staphylococcal nuclease digestion data revealed that initially most of the repair synthesis occurred in nuclease sensitive regions of chromatin. Continuous labeling experiments and pulse chase experiments indicated that with time much of the 3H dThd initially incorporated into nuclease sensitive regions during repair appeared in nuclease resistant regions. Agarose gel electrophoresis was used to demonstrate that these resistant regions were core DNA. In agreement with previous findings [Smerdon, M.J. and Lieberman, M.W., (1978), Proc. Nat. Acad. Sci. USA, in press], studies of the time course of this rearrangement and of repair synthesis revealed similar time dependences and suggested a relationship between rates of repair synthesis and chromatin rearrangement.

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Double‐strand breaks in DNA caused by repair of damage due to ultraviolet light

Bradley

1981

J. Supramol. Struct. Cell. Biochem.

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DNA DSBs are formed in normal human IMR-90 cells during repair incubation after 100 and 300 J.m-2 of UVL. By contrast, no DSBs are formed after UVL in human XPA cells that are unable to excise pyrimidine dimers. The DSBs are not due to immediate cell death since all the cells excluded trypan blue at the time of assay and because XPA cells, which are much more UVL-sensitive than IMR-90, did not form DSBs after UVL. We suggest that these repair-induced DSBs should be potent lesions that might lead to cytotoxicity, chromosome aberrations, deletion mutations, and perhaps cellular transformation. transformation.

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Heterogeneous distribution of DNA alkylation products in rat liver chromatin after in vivo administration of N,N-DI[14C]methylnitrosamine

Cited by 29 publications

References 29 publications

In vivo replication of hepatic deoxyribonucleic acid of rats treated with dimethylnitrosamine: presence of dimethylnitrosamine-induced O6-methylguanine, N7-methylguanine, and N3-methyladenine in the replicated hybrid deoxyribonucleic acid

In vivo replication of hepatic deoxyribonucleic acid of rats treated with dimethylnitrosamine: presence of dimethylnitrosamine-induced O6-methylguanine, N7-methylguanine, and N3-methyladenine in the replicated hybrid deoxyribonucleic acid

The distribution of DNA repair synthesis in chromatin and its rearrangement following damage with N-acetoxy-2-acetylaminofluorene

Double‐strand breaks in DNA caused by repair of damage due to ultraviolet light

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