The aim of this study was to examine whether an association exists between glutathione S-transferase Mu-1 (GSTM1) gene polymorphism and idiopathic male infertility.
We observed an association between male infertility and the GSTM1 and GSTT1 null deletion, but not with the CYP1A1 polymorphism in North Iranian men with idiopathic infertility.
The study showed statistically significant protective association of GSTT1 null genotype with human male infertility (odds ratio [OR]: 0.3, 95% confidence interval [CI] 0.143-0.9966, P = .048) but not with GSTM1 null genotype (OR: 0.66, 95% CI 0.3653-1.2234, P = .19).
In subgroup analysis of Caucasians, there was also an obvious association between GSTM1 null genotype and increased risk of male infertility (OR = 1.51, 95%CI 1.11-2.05, P = 0.006).
These results demonstrated that amongst populations studied to date, GSTM1 and GSTT1 null genotypes are associated with strong and modest increase in the risk of male infertility, respectively.
In conclusion, these results support that the GSTM1 null genotype mainly contributes to idiopathic male infertility susceptibility, particularly to OAT.
Overall, a significant association was seen between GSTM1 (OR=1.20, 95 % CI=1.02-1.40, P(heterogeneity) =0.000, P=0.027) genotypes and male infertility.
The results suggested that null genotypes of GSTM1 and GSTT1 are associated with spermatogenesis impairment and may contribute to susceptibility to spermatogenesis impairment and male infertility in Chinese population.
These results indicated that the null genotype of the GSTM1 gene might contribute to the susceptibility of male infertility, whereas the null genotype of the GSTT1 gene may be a genetic susceptibility factor of male infertility for the Chinese.
Further studies of GSTM1 and GSTT1 with their biological functions are needed to understand the role of these genes in the development of male infertility.
Genotype combinations GSTP1 105II/GSTT1 del (G1), GSTM1 del/GSTT1 del (G2) and GSTM1 + /GSTT1 del (G3) were associated with decreased risk of male infertility (P ≤ 0.003), whereas a genotype combination GSTP1 105IV/GSTT1 + (G4) was associated with increased disease risk (P = 0.001).
Our findings also underrate the significance of the effect of GSTM1 and/or GSTT1 (especially the former) in modulating the risk of male infertility in males from Sichuan, Southwest China.
Our meta-analysis supports that the GSTM1/GSTT1 null genotype might contribute to individual susceptibility to male infertility in Chinese populations.