Caffeine-inhibited DNA repair in 7-bromomethylbenz (a)-anthracene-treated Chinease hamster cells: formation of breaks in parental DNA and inhibition of ligation of nascent DNA as a mechanism for enhancement of lethality and chromosome damage.

The cytotoxic and clastogenic effects of 7-bromomethylbenz(a)anthracene (7-BMBA) are potentiated by post-treatment incubation of cells in the presence of an non-toxic concentration of caffeine. Under these conditions caffeine inhibits the rate of ligation of newly-synthesised DNA and induces breaks in the template strand of DNA. It is proposed that endonucleolytic attack occurs at the site of lesions in the template strand of DNA and that a later step(s) of excision-repair is (are) inhibited by the presence of caffeine-induced 'gap' in the nascent DNA opposite these lesions.