Genomic damage induced in tobacco plants by chlorobenzoic acids--metabolic products of polychlorinated biphenyls.

Tobacco seedlings (Nicotiana tabacum var. xanthi) were treated for 24 h with mono-(2- and 3-CBA), di-(2,5- and 3,4-CBA), and tri-(2,4,6- and 2,3,5-CBA)-chlorobenzoic acids (CBAs) and with the mixture of polychlorinated biphenyls--Delor 103, or cultivated for 1 or 2 weeks in soil polluted with the CBAs. DNA damage in nuclei of leaves and roots was evaluated by the comet assay.

Evaluation of DNA damage and mutagenicity induced by lead in tobacco plants.

Tobacco (Nicotiana tabacum L. var. xanthi) seedlings were treated with aqueous solutions of lead nitrate (Pb2+) at concentrations ranging from 0.

Monitoring toxicity, DNA damage, and somatic mutations in tobacco plants growing in soil heavily polluted with polychlorinated biphenyls.

Heterozygous tobacco (Nicotiana tabacum var. xanthi) plants were cultivated in soil from a dump site highly polluted with polychlorinated biphenyls (PCBs) at Lhenice in South Bohemia, Czech Republic. The total amount of PCBs in the polluted soil, measured by gas chromatography varied from 165 to 265mgkg(-1) of soil.

DNA staining with the fluorochromes EtBr, DAPI and YOYO-1 in the comet assay with tobacco plants after treatment with ethyl methanesulphonate, hyperthermia and DNase-I.

We applied the alkaline version of the single-cell gel electrophoresis (comet) assay to roots and leaves of tobacco (Nicotiana tabacum var. xanthi) seedlings or isolated leaf nuclei treated with: (1) the alkylating agent ethyl methanesulphonate, (2) necrotic heat treatments at 50 degrees C, and (3) DNase-I. All three treatments induced a dose-dependent increase in DNA migration, expressed as percentage of tail DNA.

Toxicity and DNA damage in tobacco and potato plants growing on soil polluted with heavy metals.

Heterezygous tobacco (Nicotiana tabacum var. xanthi) and potato (Solanum tuberosum var. Korela) plants were cultivated on soil from the site Strimice which is highly polluted with heavy metals and on nonpolluted soil from the recreational site Jezerí, both in North Bohemia, Czech Republic.

Evaluation of the nuclear DNA Diffusion Assay to detect apoptosis and necrosis.

We applied the nuclear DNA Diffusion Assay, described as an accurate tool to estimate apoptotic and necrotic cells [N.P. Singh, A simple method for accurate estimation of apoptotic cells, Exp.

Cadmium induces DNA damage in tobacco roots, but no DNA damage, somatic mutations or homologous recombination in tobacco leaves.

The heavy metal cadmium (Cd(2+)) applied on tobacco roots in the form of cadmium chloride, induced significantly higher levels of DNA damage as measured by the cellular Comet assay than did treatment of isolated root nuclei, analyzed by use of the acellular Comet assay. DNA damage induced by Cd(2+) in roots of a transgenic catalase-deficient tobacco line (CAT1AS) was higher than in wild-type tobacco (SR1) roots. In contrast to treatment with the positive control ethyl methanesulphonate, Cd(2+) induced no significant DNA damage in leaf nuclei, and neither somatic mutations, nor homologous recombination as measured by the GUS genereactivation assay, were observed in leaves.

Differential genotoxicity of ethyl methanesulphonate, N-ethyl-N-nitrosourea and maleic hydrazide in tobacco seedlings based on data of the Comet assay and two recombination assays.

The purpose of this study was to determine if mutagen-induced DNA damage is correlated with the frequency of induced recombination events. The alkylating agents ethyl methanesulphonate (EMS) and N-ethyl-N-nitrosourea (ENU), and the plant growth regulator and herbicide maleic hydrazide (MH) were compared in tobacco seedlings for their ability to induce DNA damage measured by the Comet assay, and recombination activity measured by the GUS gene reactivation assay, and by the somatic twin sectors assay. While EMS and ENU induced a dose-dependent increase in DNA damage in leaf nuclei, MH had no significant effect.

DNA damage induced by indirect and direct acting mutagens in catalase-deficient transgenic tobacco. Cellular and acellular Comet assays.

We have measured the level of DNA damage induced by treating roots (cellular Comet assay) and isolated root nuclei (acellular Comet assay) of catalase-deficient (CAT1AS) and wild-type (SR1) tobacco with the promutagen o-phenylenediamine (o-PDA) and the direct acting genotoxic agents hydrogen peroxide and ethyl methanesulphonate (EMS). The roots of CAT1AS have about 60% less catalase activity compared to the roots of SR1. The promutagen o-PDA applied on tobacco roots induced significantly higher levels of DNA damage in the CAT1AS transgenic line than in SR1, while after application of o-PDA on isolated root nuclei, no DNA damage could be detected.

Monitoring DNA damage in wood small-reed (Calamagrostis epigejos) plants growing in a sediment reservoir with substrates from uranium mining.

For most plant species growing in polluted areas genotoxicity assays are not available. We have studied the possibility of using the alkaline protocol of the Comet assay as a method for detecting induced DNA damage in a grass Calamagrostis epigejos, growing wild in highly polluted areas. To calibrate the Comet assay for C.

DNA damage induced by hydrogen peroxide in cultured tobacco cells is dependent on the cell growth stage.

The level of hydrogen peroxide (H(2)O(2))-induced genomic DNA damage measured by the Comet assay in tobacco suspension cells (TX1) increased as a function of the age of the culture. After treatment of TX1 cells with 15 mM H(2)O(2), the average (+/-S.E.