Abstract
The genotoxicity of cyproterone acetate was studied in human lymphocytes using chromosomal aberrations (CAs), mitotic index (MI) and sister chromatid exchanges (SCEs) as a parameter. Cyproterone acetate was found to be genotoxic at 20 and 30 microM. To study the possible mechanism of the genotoxicity of cyproterone acetate, superoxide dismutase (SOD) and catalase (CAT) were used separately and in combination along with the 30 microM of cyproterone acetate at different doses. SOD treatment increases CAs, SCEs and decreases MI as compared to treatment with 30 microM CPA alone, at both of the tested doses. CAT treatment decreases the frequencies of CAs and SCEs and increases MI in both, as compared to treatment with 30 microM CPA alone, separately and in combination with SOD, suggesting a possible role of reactive oxygen species for the genotoxic damage.