Induction of chromosomal aberrations and sister chromatid exchanges by chlormadinone acetate in human lymphocytes: A possible role of reactive oxygen species

Abstract

Genotoxicity study of a synthetic progestin chlormadinone acetate (CMA) was carried out in human lymphocytes using chromosomal aberrations (CAs) and sister chromatid exchanges (SCEs) as parameter. Effect of CMA was studied at 10, 20, 30 and 40 μ<i>M. </i>CMA was genotoxic at 30 and 40 μ<i>M. </i>With a view to study the possible mechanism of genotoxicity of CMA, superoxide dismutase (SOD) and catalase (CAT) were used separately and in combination along with the CMA (40 μ<i>M</i>)<i> </i>at different doses. SOD treatment increased CAs and SCEs at both the doses. CAT treatment decreased the frequencies of CAs and SCEs in both, separately and in combination with SOD, suggesting a possible role of reactive oxygen species for the genotoxic damage.