Many studies have reported on the association between GST ge

Many studies have reported on the association between GST gene polymorphisms and pulmonary disorders but with controversial results [7]. In the present study, on comparing results of GSTP1 gene polymorphism among the studied COPD patient groups, it was found that heterozygote mutation was significantly higher in group A (COPD smokers) than in group B (COPD non smokers). This result comes in accordance with Bentley et al. [10] who declared that in GSTP1, the heterozygous mutation due to substitution of Ile amino Moniliformin sodium salt at codon number 105 by Val which causes altered affinity for specific substrates, was associated with chronic smoking COPD patients (Table 3). Similarly, Lakhdar et al. [2] found the Tunisians carrying a GSTP1 Val105 allele were at higher risk of COPD. In addition, the meta-analysis completed by Yan et al. [11] suggested that the GSTP1 105Val/Val genotype was an important genetic contributor to COPD susceptibility. In contrast, Yim et al. [12] showed no association between GSTP1 gene polymorphism at exon 5 and COPD in Koreans, while Ishii et al. [13] showed an increased prevalence of homozygous mutation (similar alleles) in GSTP1 polymorphism at exon 5 in Japanese COPD patients. Regarding (Table 4) of the current study, the number of detected GSTP1 mutations was significantly higher in smoking patients than those not smoking or quit smoking. Out of twenty-five heterozygous mutations detected, eleven subjects were smoking (41.7%), six were not smoking (25%) and eight were ex-smokers (33.3%). This result comes in accordance with Spira [14] who stated that some people who smoke respond differently at a genetic level to a cigarette smoke. These people may be at a heightened risk of developing COPD because genes that normally protect lung cells against environmental toxins are altered, including some genes linked to COPD. Moreover, Zuntar et al. [7] reported that there were no significant differences between healthy smokers and COPD-smokers. Regarding (Table 5), the current study showed no significant difference between studied subjects having heterozygous mutation and subjects without as regards spirometry results. This result comes in accordance with the International Journal of COPD., [15] a study search that identified 104 publications reporting a total of 130 genes and 48 intergenic regions studied in 20,288 individuals including GSTP1 exon 5 polymorphism. This great study declared that none of the studied genes was significantly associated with forced expiratory volume in one second (FEV1) or FEV/forced vital capacity (FVC) ratio after correction for multiple testing. Moreover, Rodriguez et al. [16] declared that no significant association was observed in different genotypes of the GSTP1 with lung function in the group of patients with COPD. They reported that the GSTP1 genotypes studied did not seem to influence the severity of lung function impairment in patients with COPD. However, in a large study designed by He et al. [17] involving 1098 individuals with different degrees of lung function impairment, the results demonstrated a significant association of mutation with rapid decline in lung function in smokers with mild to moderate airflow obstruction.
Conclusion
Conflict of interest
Introduction Glutathione S-transferases (GSTs, EC.2.5.1.18) are a family of multifunctional enzymes that play a crucial role in cellular detoxification by catalyzing the nucleophilic addition of glutathione to a broad range of endogenous and exogenous hydrophobic electophilic compounds [1]. GSTs are dimeric proteins which are classified into seven cytosolic classes (α, μ, π, θ, ω, σ, ξ), one mitochondrial family (κ) and one microsomal membrane-bound family [2], [3]. The human pi class of GST, GSTP1-1, is frequently involved in the formation and the progression of tumors [4], [5] so that its over-expression is a common feature of many human tumors of a wide range of tissues including, blood, stomach, brain and colon [6], [7], [8], [9], [10] and that a high level of GSTP1-1 expression is a bad prognostic for patient survival [11]. In addition, GSTP1-1 is involved in resistance against antineoplastic drugs [12], [13], [14] and inhibits apoptosis by binding to the Jun N-terminal Kinase (JNK) [15]. However, in normal cells, increased GSTP1-1 expression is frequently associated with conditions of physiological cellular stress [1].