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Aim of work: To study the genetic variants of glutathione S-transferases and monocyte CD64 expression in systemic lupus erythematosus patients and to evaluate their role in disease susceptibility, activity and damage. Patients and methods: Forty female SLE patients and 40 age matched controls were genotyped for GSTP1, GSTM1 and GSTT1 gene polymorphisms using polymerase chain reaction-restriction fragment length polymorphism, conventional PCR and were assessed for monocyte CD64 expression level using flow cytometry. SLE disease activity index (SLEDAI) and the systemic lupus international. collaborating clinics/damage index (SLICC DI) were considered. Results: The patients mean age was 28.13 ± 4.56 years and disease duration of 6.4 ± 4.9 with a SLEDAI of 14.4 ± 7.1 and SLICC/DI 3.7 ± 1.5. The frequency of GSTM1 null genotype tended to be higher (55%) in SLE patients compared to the controls (and 42.5%) (p = 0.09). The frequency of GSTT1 null genotype was significantly higher in SLE patients (25%) compared to controls (12.5%) (p

Oxidative stress was related with carpal tunnel syndrome (CTS). We aimed to clarify the associations between glutathione S-transferase (GST)M1, GSTT1 and GSTP1-Ile105Val polymorphisms and CTS. One hundred-forty patients with CTS and 97 healthy controls were enrolled in this study. Tinel and Phalen signs were noted as positive or negative. Functional and clinical status of patients was evaluated by the Boston Questionnaire. The intensity of hand and/or wrist pain was evaluated on 10 cm visual analog scale (VAS). We applied the polymerase chain reaction (PCR) to determine the polymorphisms of the GSTM1 and GSTT1 and the PCR-restriction fragment length polymorphism method for detecting the GSTP1-Ile105Val polymorphism. The M1 null genotype was significantly higher in patients with CTS compared to healthy controls, and the M1 null genotype seemed to increase the risk of CTS approximately two-fold (P = 0.011; odds ratio (OR) = 1.98; 95 % confidence interval (CI) 1.17-3.36). The M1 null, T1 present combined genotype was significantly higher in patients with CTS compared to healthy controls (P = 0.043); however, it seemed not to increase the risk of CTS (P = 0.14; OR = 0.62; 95 % CI 0.33-1.76). We found significantly higher levels of the VAS, Boston Symptom Severity Scale and Phalen sign in patients with the Ile/Val or the Val/Val genotypes compared to those in patients with the Ile/Ile genotype (P = 0.003, 0.004 and 0.044, respectively). We proposed that genes involved in the protection from oxidative stress may influence the susceptibility, clinical and functional status of CTS. The GSTM1 null genotype may be related with the development of CTS, whereas the Val allele of GSTP1-Ile105Val polymorphism may be associated with worse functional and clinical status in CTS.

A common feature of environmental irritants is their ability to cause local inflammation which could alter airway function. The principal targets of such injury are the epithelial cells lining the airway passages and the lower respiratory gas-exchange areas. While host atopy is a recognized risk factor for airway inflammation, atopy alone cannot cause asthma. We hypothesize that susceptibility to persistent airway inflammation in atopic individuals is characterized by an inherited deficiency in the effectiveness of detoxification of inhaled irritants and products of oxidative stress such as reactive oxygen species (ROS). Our case-control studies show that polymorphisms at the glutathione S-transferase, GSTP1, locus on chromosome 11q13 may account for variation in host response to oxidative stress, a key component of airway inflammation. Frequency of the GSTP1 Val/Val genotype is reduced in atopic subjects compared with nonatopic subjects. Trend analysis also shows a significant decrease of GSTP1 Val/Val (with parallel increase of GSTP1 Ile/Ile) genotype frequency with increasing severity of airflow obstruction/bronchial hyperresponsiveness. The implication of specific polymorphisms at the GSTP1 locus in airway inflammation is entirely novel: however, GST are recognized as a supergene family of enzymes critical in 1) cell protection from the toxic products of ROS-mediated reactions, 2) modulation of eicosanoid synthesis.