Sister chromatid exchange (SCE) and chromosome aberrations (CA) in peripheral lymphocytes has been widely used in assessing exposure to mutagens and carcinogens. One of the extensively studied genotoxins is benzo[alpha]pyrene (BaP). We studied the ability of BaP to induce SCE and CA in 16 glutathione S-transferase M1 (GSTM1)-positive and 15 GSTM1-null individuals by analyzing 72-h whole-blood lymphocyte cultures, either BaP-untreated (controls) or treated with 5 µM of BaP for 24 or 48 h. There was no differences in the level of BaP-induced chromosomal aberrations between GSTM1-positive or null individuals when the cells were BaP-exposed for 24 h (0.083 ± 0.059 vs. 0.090 ± 0.058) or 48 h (0.092 ± 0.057 vs. 0.096 ± 0.050. The frequency of SCE in controls was GSTM1-positive = 2.96 ± 0.35 and GSTM1-null = 3.23 ± 0.56 while that for BaP-treated lymphocytes was GSTM1-positive = 5.56 ± 0.83 and GSTM1-null = 6.09 ± 1.11 and were not statistically significant. The rates of BaP-induced in vitro chromatid and chromosome-type gaps and breaks were similar in all groups, although GSTM1-null genotype chromatid-type breaks were more frequent (0.064 ± 0.039 per metaphase) than chromosome-type breaks (0.032 ± 0.027 per metaphase) after 48 h treatment with BaP (p < 0.001). These findings suggest that BaP-induced in vitro SCE and CA are not influenced by the GSTM1 genotype.
sister chromatid exchanges; chromosomal aberrations; benzo[alpha]pyrene; glutathione S-transferase M1