Purpose

This study aimed to explore the effects of genetic polymorphisms in metabolic enzymes on relative telomere length changes and explore the mechanism of canceration induced by omethoate.

Materials and Methods

180 long-term omethoate-exposed workers and 115 healthy controls were recruited. Real-time PCR method was applied to determine the relative telomere length in peripheral blood leukocytes DNA, and Six polymorphic loci of GSTT1 (+/−), GSTM1 (+/−), GSTP1 rs1695, CYP2E1 rs6413432, CYP2E1 rs3813867 and PON2 rs12026 were detected by polymerase chain reaction and restriction fragment length polymorphism method; Multiple linear regression was conducted to explore the effects of omethoate exposure and genetic polymorphisms on the telomere length.

Results

The relative telomere lengths in the control group (0.94 [0.76, 1.32]) were significantly shorter than that in the exposure group (1.50 [1.11, 2.57])(Z= 7.910, P< 0.001). Univariate analysis showed that the relative telomere lengths of the GSTM1-deletion individuals were significantly longer than that of the non-deletion genotype in the control group (Z= 2.911, P= 0.004), and the relative telomere lengths of GSTP1 rs1695 polymorphism locus (GG+ AG) genotype individuals were longer than that of AA genotype in the exposure group. The difference was statistically significant (Z= 2.262, P= 0.024). Multivariate analysis found that pesticide-exposure (b= 0.524, P< 0.001) and GSTM1 polymorphism (b=− 0.136, P= 0.029) had an impact on telomere length.

Conclusions

The relative telomere lengths of omethoate-exposure workers were longer than that in the control population. Also GSTM1 genetic polymorphism may influence the changes of the telomere length induced by omethoate.