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Comparative genotoxicity of the herbicides Roundup, Stomp and Reglone in plant and mammalian test systems
Author(s) -
B. D. Dimitrov,
P. Gadeva,
D. Benova,
M. V. Bineva
Publication year - 2006
Publication title -
mutagenesis
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.723
H-Index - 91
eISSN - 1464-3804
pISSN - 0267-8357
DOI - 10.1093/mutage/gel044
Subject(s) - micronucleus test , genotoxicity , biology , bone marrow , diquat , micronucleus , mitosis , genetics , microbiology and biotechnology , immunology , chemistry , toxicity , biochemistry , paraquat , organic chemistry
The genotoxicities of the herbicides Roundup (glyphosate), Stomp (pendimethaline) and Reglone (diquat), were compared in plant (Crepis capillaris L.) and mouse bone marrow test systems using chromosomal aberrations and micronuclei. Roundup did not induce chromosomal aberrations or micronuclei in either test system. Reglone also did not induce chromosomal aberrations in either test system; however, it increased micronucleus frequency in both plant cells and mouse bone marrow polychromatic erythrocytes (PCEs). The responses of the two test systems to Stomp were quite different. Stomp did not induce chromosomal aberrations in the plant cells, but increased their incidence in mouse cells; Stomp increased the frequency of micronuclei in both test systems. The induction of micronuclei in plant cells may have been due to the spindle-destroying effect of the herbicide, since all concentrations of Stomp produced C-mitoses. The increased chromosomal aberration frequency in mouse bone marrow cells observed at later sampling times after administration of Stomp into animals suggests that the induction of aberrations may be due to biosynthesis of genotoxic metabolites. This conclusion was supported by the coincidence between the frequencies of chromosomal aberrations and of micronucleated PCEs in mouse cells. These data indicate that plant and animal assays are differentially responsive to some pesticides, and these differences may be due to metabolism and their responses to mitotic spindle disruption.

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