Glutathione- S -transferase (GST) theta polymorphism influences background SCE rate

Polymorphism of glutathione S-transferase θ (GSTT1) modulates the toxicity of halogenated alkanes and epoxides in humans. The enzymatic activity of glutathione S-transferase θ and its corresponding gene is lacking in about 30% of the central European population. It has now been demonstrated that the background rate for sister chromatid exchange (SCE) is affected by this particular polymorphism. Smoking as a known inducer of SCE was taken into account. A group of GSTT1-positive subjects exhibited lower SCE rates than GSTT1-negative individuals (7.55±0.77 versus 8.74±1.24 SCE/mitosis, respectively, p<0.005). Non-smoking GSTT1-positive individuals showed the lowest SCE rate (7.26±0.71 SCE/mitosis), significantly lower than the rates of smoking GSTT1-positive and non-smoking GSTT1-negative subjects (8.14±0.55 SCE/mitosis and 8.12±0.88 SCE/mitosis, respectively, p<0.025 in both cases). Smoking GSTT1-negative subjects exhibited the highest SCE rates (9.28±1.3 SCE/mitosis). It is hypothesized that GSTT1 is protective against background genotoxic damage. Since ethylene oxide is a proven substrate of GSTT1, the detoxification of this epoxide arising from endogenous ethylene may modulate SCE background rates.