Abstract
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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