By: Norma V. González, Sonia Soloneski, Marcelo L.
Larramendy
The sister chromatid exchange (SCE) frequency, the cell-cycle progression analysis, and the single cell gel electrophoresis technique (SCGE, comet assay) were employed as genetic end-points to investigate the geno- and citotoxicity exerted by dicamba and one of its commercial formulation banvel (dicamba 57.71%) on Chinese hamster ovary (CHO) cells. Log-phase cells were treated with 1.0–500.0 μg/ml of the herbicides and harvested 24 h later for SCE and cell-cycle progression analyses. All concentrations assessed of both test compounds induced higher SCE frequencies over control values. SCEs increased in a non-dose-dependent manner neither for the pure compound (r = 0.48; P > 0.05) nor for the commercial formulation (r = 0.58, P > 0.05). For the 200.0 μg/ml and 500.0 μg/ml dicamba doses and the 500.0 μg/ml banvel dose, a significant delay in the cell-cycle progression was found. A regression test showed that the proliferation rate index decreased as a function of either the concentration of dicamba (r = −0.98, P < 0.05) or banvel (r = −0.88, P < 0.01) titrated into cultures in the 1.0–500.0 μg/ml dose-range. SCGE performed on CHO cells after a 90 min pulse-treatment of
dicamba and banvel within a 50.0–500.0 μg/ml dose-range
revealed a clear increase in dicamba-induced DNA damage as an enhancement of the
proportion of slightly damaged and damaged cells for all concentrations used (P
< 0.01); concomitantly, a decrease of undamaged cells was found over control
values (P < 0.01). In banvel-treated cells, a similar overall result was
registered. Dicamba induced a significant increase both in comet length and
width over control values (P < 0.01) regardless of its concentration whereas
banvel induced the same effect only within 100.0–500.0 μg/ml dose range (P <
0.01). As detected by three highly sensitive bioassays, the present results
clearly showed the capability of dicamba and banvel to induce DNA and cellular
damage on CHO cells.
The sister chromatid exchange (SCE) frequency, the cell-cycle progression analysis, and the single cell gel electrophoresis technique (SCGE, comet assay) were employed as genetic end-points to investigate the geno- and citotoxicity exerted by dicamba and one of its commercial formulation banvel (dicamba 57.71%) on Chinese hamster ovary (CHO) cells. Log-phase cells were treated with 1.0–500.0 μg/ml of the herbicides and harvested 24 h later for SCE and cell-cycle progression analyses. All concentrations assessed of both test compounds induced higher SCE frequencies over control values. SCEs increased in a non-dose-dependent manner neither for the pure compound (r = 0.48; P > 0.05) nor for the commercial formulation (r = 0.58, P > 0.05). For the 200.0 μg/ml and 500.0 μg/ml dicamba doses and the 500.0 μg/ml banvel dose, a significant delay in the cell-cycle progression was found. A regression test showed that the proliferation rate index decreased as a function of either the concentration of dicamba (r = −0.98, P < 0.05) or banvel (r = −0.88, P < 0.01) titrated into cultures in the 1.0–500.0 μg/ml dose-range. SCGE performed on CHO cells after a 90 min pulse-treatment of
dicamba and banvel within a 50.0–500.0 μg/ml dose-range
revealed a clear increase in dicamba-induced DNA damage as an enhancement of the
proportion of slightly damaged and damaged cells for all concentrations used (P
< 0.01); concomitantly, a decrease of undamaged cells was found over control
values (P < 0.01). In banvel-treated cells, a similar overall result was
registered. Dicamba induced a significant increase both in comet length and
width over control values (P < 0.01) regardless of its concentration whereas
banvel induced the same effect only within 100.0–500.0 μg/ml dose range (P <
0.01). As detected by three highly sensitive bioassays, the present results
clearly showed the capability of dicamba and banvel to induce DNA and cellular
damage on CHO cells.
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