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鞣酸对黑腹果蝇体细胞中丝裂霉素C、甲基磺酸甲酯和氮芥遗传毒性的干扰作用。

Interference of tannic acid on the genotoxicity of mitomycin C, methylmethanesulfonate, and nitrogen mustard in somatic cells of Drosophila melanogaster.

作者信息

Lehmann M, Graf U, Reguly M L, Rodrigues De Andrade H H

机构信息

Laboratory of Mutagenesis, Department of Genetics, Federal University of Rio Grande do Sul, Porto Alegre, Rio Grande do Sul, Brazil.

出版信息

Environ Mol Mutagen. 2000;36(3):195-200. doi: 10.1002/1098-2280(2000)36:3<195::aid-em2>3.0.co;2-b.

DOI:10.1002/1098-2280(2000)36:3<195::aid-em2>3.0.co;2-b
PMID:11044900
Abstract

The modulating effects of tannic acid (TA) on somatic mutation and mitotic recombination induced by methylmethanesulfonate (MMS), nitrogen mustard (HN2), and mitomycin C (MMC) were evaluated in the standard (ST) cross of the wing spot test in Drosophila melanogaster using co- and posttreatment protocols. It was shown that TA alone did not modify the spontaneous frequencies of single and twin spots, which means that this polyphenol neither acts as a genotoxin nor exerts any antigenotoxic effect over spontaneous DNA lesions. However, the simultaneous administration of genotoxins with TA can lead to considerable alterations of the frequencies of induced wing spots in comparison to those with administration of the genotoxins alone. In fact, TA produced a significant increase in HN2-induced wing spots with enhancements between 90 and 160%. For MMS, the enhancement was 38% in the highest TA concentration tested. In contrast, a significant protective action of this polyphenol was observed in combined treatments with MMC (64 to 99% inhibition). Moreover, the data from TA posttreatments demonstrated that this agent is not effective in exerting protective or enhancing effects on the genotoxicity of MMS, HN2, or MMC. One feasible mechanism of TA action is its interaction with the enzyme systems catalyzing the metabolic detoxification of MMS and HN2, which may also be involved in the bioactivation of MMC.

摘要

采用共处理和后处理方案,在黑腹果蝇翅斑试验的标准杂交中评估了单宁酸(TA)对甲磺酸甲酯(MMS)、氮芥(HN2)和丝裂霉素C(MMC)诱导的体细胞突变和有丝分裂重组的调节作用。结果表明,单独使用TA不会改变单斑和双斑的自发频率,这意味着这种多酚既不充当基因毒素,也不会对自发DNA损伤产生任何抗基因毒性作用。然而,与单独使用基因毒素相比,基因毒素与TA同时给药可导致诱导翅斑频率发生显著变化。事实上,TA使HN2诱导的翅斑显著增加,增幅在90%至160%之间。对于MMS,在测试的最高TA浓度下增幅为38%。相反,在与MMC的联合处理中观察到这种多酚具有显著的保护作用(抑制率为64%至99%)。此外,TA后处理的数据表明,该试剂对MMS、HN2或MMC的基因毒性没有有效的保护或增强作用。TA作用的一种可行机制是其与催化MMS和HN2代谢解毒的酶系统相互作用,这也可能参与MMC的生物活化。

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