ABSTRACT
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 æM 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.