PHOTOSENSITIZED INACTIVATION OF INFECTIOUS DNA BY UROCANIC ACID, INDOLEACRYLIC ACID AND RHODIUM COMPLEXES

Naked, infectious single-stranded (ss) and double-stranded (ds) DNA fr om phages S13 and G4 were irradiated with 308 nm UV radiation in the a bsence and presence of several photobiologically active compounds: E- and Z-urocanic acid (E- and Z-UA), their methyl esters (E- and Z-MU), E- and Z-indoleacrylic acid (E- and Z-IA), cis-dichlorobis(1,10-phenan throline)rhodium (III) chloride (cDCBPR) and tris(1,10-phenanthroline) rhodium (III) perchlorate (TPR). E-urocanic acid protects against cycl obutane pyrimidine dimer formation in ssDNA but concomitantly photosen sitizes the formation of other lesions that inactivate ssDNA. Z-urocan ic acid also protects ssDNA against such dimerization but without the associated sensitized damage. The methyl ester isomers behave similarl y. There is no such differential activity observed for the IA isomers, both of which sensitize the inactivation of ssDNA. Photostationary st ate mixtures of both UA and IA efficiently sensitize the inactivation of dsDNA, and cDCBPR strongly protects ssDNA from UV damage, while TPR is a significant sensitizer. Both of these metal complexes sensitize the inactivation of dsDNA slightly. For all compounds, cyclobutane pyr imidine dimers were the predominant lethal lesions produced by sensiti zation of the dsDNA, but they were not the major lethal lesions create d by sensitization of the ssDNA. In the case of dsDNA, both UA and IA created pyrimidine dimers with a high degree of potential for mutagene sis, as determined by an assay that monitors the frequency of mutation s following the spontaneous deamination of cytosine in photodimers.