4.1 Article

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

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ELSEVIER SCIENCE BV
DOI: 10.1016/S1383-5718(01)00204-2

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chlorophyll mutations; comet assay; ethyl methanesulphonate; o-, m- and p-Phenylenediamine; Nicotiana tabacum; single cell gel electrophoresis

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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 mu mol m(-2) s(-1) photosynthetic photon fluence, rate) during a 72 h 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. (C) 2001 Elsevier Science B.V. All rights reserved.

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