Mutagenicity of cross‐links and monoadducts of furocoumarins (psoralen and angelicin) induced by 360‐nm radiation in excision‐repair‐defective and radiation‐insensitive strains of saccharomyces cerevisiae

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Abstract
The furocoumarin psoralen can form both monoadducts and cross‐links with DNA when combined with 360‐nm radiation, whereas the analog angelicin can form monoadducts only. Psoralen plus 360‐nm radiation causes mutation induction with a slope of 2 (log‐log plot) for a radiation‐insensitive strain, whereas angelicin action with 360‐nm radiation displays a slope of unity. For a radiation‐sensitive mutant defective in the excision‐repair pathway, the actions of both angelicin and psoralen plus 360‐nm radiation exhibit one‐target kinetics, but at higher exposures psoralen plus 360‐nm radiation assumes a slope of 2. The excision‐repair‐defective strain is considerably more sensitive to the furocoumarins plus 360‐nm radiation than is the radiation‐insensitive strain, both for killing and mutation induction. The simplest explanation for the data is that both cross‐links and monoadducts, formed by furocoumarins with DNA when exposed to 360‐nm radiation, are capable of inducing mutations, and that monoadducts are repaired 20 times more efficiently than cross‐links by the excision‐repair pathway.

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