02388nas a2200241 4500000000100000008004100001653008600042100001500128700002500143700002200168700002000190700002400210700001400234700002100248700001700269700002100286700002600307245009500333856005100428300001200479490000700491520164800498 2016 d10aGlutathione S-transferase; Leprosy; Reactive Oxygen Species; Mycobacterium leprae1 aGraça C R1 aCordeiro-Soubhia R M1 aTonelli-Nardi S M1 aBelini Junior E1 aBonini-Domingos C R1 aGauch C R1 aDa Rocha E M D S1 aPaschoal V D1 aKouyoumdjian J A1 aDe Souza Baptista A R00aIs nullity for Glutathione S-transferase genes GSTT1 and GSTM1 protective against leprosy? uhttps://leprosyreview.org/article/87/2/23-2238 a232-2380 v873 a

Introduction: Leprosy is a slow and progressive infectious disease caused by Mycobacterium leprae. The generation of free radicals called reactive oxygen species (ROS), which promote destruction of the bacillus within macrophages, is an effective defence mechanism developed by the host. In parallel, the glutathione S-transferase (GST) multifamily of enzymes constitutes an important antioxidant system for ROS detoxification and protection against toxicity. Therefore, GST null genotype individuals could reduce the detoxification of ROS, increasing host effectiveness for M. leprae destruction.

Objectives: To evaluate polymorphisms in the GSTT1 and GSTM1 genes as human leprosy susceptibility modulators. 

Methods: GSTT1 and GSTM1 polymorphisms were genotyped by a multiplex polymerase chain reaction (PCR) in 218 leprosy patients and 244 non-leprosy subjects (control group).

Results: The occurrence of the GSTT1/GSTM1 null genotype was significantly higher among control subjects than amongst leprosy patients (P ¼ 0·01). The GSTT1 positive genotype frequency was significantly increased in leprosy patients when compared with control subjects (P ¼ 0·01).

Conclusions: The results suggest that GSTT1/M1 nullity may play an important role in leprosy pathogenesis.

Significance: Despite these findings, further studies will be necessary to ascertain the exact role of these genes in leprosy and to design any future prevention measures or contributions to drug therapy.