We have investigated the genotoxic activity of rotenone on three genetic endpoints, sister-chromatid exchanges (SCE), chromosome aberrations (CA) and micronuclei (MN) in human lymphocyte cultures in the presence and absence of a metabolic activation system (S9 mix). Our results indicate that rotenone increases the frequency of binucleated micronucleated (BNMN) cells and causes a delay in the cell cycle but does not increase the frequency of CA and SCE at the concentrations used. The presence of S9 mix reduces the genotoxic activity of rotenone.
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http://dx.doi.org/10.1016/s1383-5718(98)00032-1 | DOI Listing |
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