o-Phenylenediamine-induced DNA damage and mutagenicity in tobacco seedlings is light-dependent.

Of the three isomers of the aromatic amine phenylenediamine (PDA), only o-PDA, but not m- and p-PDA, induced DNA damage (as measured by the Comet assay), and somatic mutations in the leaves of the chlorophyll-deficient tester strain Nicotiana tabacum var. xanthi. With increasing light intensity (0, 30, 80 or 140 micromol m(-2)s(-1) photosynthetic photon fluence rate) during a 72h mutagenic treatment of tobacco seedlings, o-PDA-induced DNA damage and the yield of somatic mutations were significantly increased. The peroxidase inhibitor diethyldithiocarbamate (DEDTC) repressed o-PDA-induced DNA damage. The effect of light is caused by the light-dependent increase of peroxidase activity and the accumulation of hydrogen peroxide, which participate in the metabolic activation of the promutagen o-PDA to mutagenic product(s). In contrast, DNA damage induced by the direct-acting alkylating mutagen ethyl methanesulphonate was the same whether treatment was in the light or in the dark, and was not repressed by the peroxidase inhibitor DEDTC.