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Nucleic Acids Research, 1981, Vol. 9, No. 21 5533-5552
© 1981

MOLECULAR BIOLOGY

The distribution of benzo(a)pyrene DNA adducts in mammalian chromatin

Peter L. Jack and Peter Brookes

Chemical Carcinogenesis Division, Institute of Cancer Research, Pollards Wood Research Station, Nightingales Lane Chalfont St. Giles, Bucks HP8 4SP, UK

Received August 24, 1981. This paper describes the distribution of DNA-lesions generated by the potent carcinogen benzo(a)pyrene (BP) or its ultimate metabolic derivative 7{alpha}, 8ß, di-hydroxy-9ß, 10ß-epoxy-7,8,9,10-tetrahydrobenzo(a)pyrene (BPDE) within mammalian chromatin using the enzymic probe micrococcal nuclease. We have shown that the progress of the nuclease on naked DNA is unaffected by the presence of the hydrocarbon lesion at moderate extents of digestion. Digestion of nuclei isolated from murine erythroleukaemic cells immediately following BPDE treatment, and analysis of micrococcal nuclease resistant DNA by TCA precipitation, hydroxyapatite chromatography and gelelectrophoresis demonstrates a non-random distribution of lesions. Approximately three times more binding occurs on the linker DNA regions between nucleosome cores than on the nucleosome core DNA itself. A similar result was obtained with BPDE treated primary mouse embryo cells; however nuclei isolated from these cells after prolonged treatment with BP (to allow metabolic activation) showed no such preferential binding. Post-treatment incubation of BPDE-treatedcells shows that this difference can be accounted for by the loss of preferential localisation with time.


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