ABSTRACT
The ability of butachlor to induce cytotoxicity, clastogenicity and DNA damage was assessed using Chinese hamster ovary cells (CHO), Swiss mouse embryo fibroblasts (MEF) and human peripheral blood lymphocytes. A dose and time dependent loss of viability was evident upon treatment of CHO cells with butachlor. Cell killing to an extent of 50% was observed when cells were treated with 16.2 micrograms/ml of butachlor for 24 hr or with 11.5 micrograms/ml for 48 hr. The herbicide induced micronuclei significantly in cultured lymphocytes at 24 and 48 hr of treatment suggesting that it is clastogenic. To understand the mechanism of cell death caused by butachlor, its effect on DNA strand breaks was studied in MEF. A concomitant decrease in cell viability was observed with increase in DNA strand breaks. Agarose gel electrophoresis of DNA from herbicide treated CHO cells and cytochemical staining indicate the induction of apoptosis by butachlor.
Subject(s)
Acetanilides/toxicity , Animals , CHO Cells , Cells, Cultured , Cricetinae , Embryo, Mammalian/cytology , Fibroblasts/drug effects , Herbicides/toxicity , Humans , Mice , Mutagens/toxicityABSTRACT
Cultured Chinese hamster ovary (CHO) cells were pre-treated with m-AMSA (amsacrine) and post-treated with different doses of polycationic compound poly-D-lysine (PDL) during G2 period in order to test on the frequency of chromatid-type aberrations. The present results indicate that PDL enhances the genotoxic action of m-AMSA measured as induced chromatid aberrations.