BACKGROUND: Multiple sclerosis (MS) occurs as a result of interaction between genetic and environmental factors. Recent data support the view that oxidative damage is one of an early event in MS tissue injury. The safe elimination of reactive oxygen species and toxins via glutathione S-transferase (GST) pathways is required in order to protect cells against reactive oxygen-induced damage. The aim of our study was to analyze the possible association of GSTM1 and GSTT1 gene polymorphisms with the susceptibility and clinical parameters of MS, in 455 consecutive patients and 366 controls. METHODS: A multiplex polymerase chain reaction (PCR) was used to detect the deletions in GSTM1 and GSTT1 genes. RESULTS: Patients with MS had significantly higher frequency of GSTT1 null genotype compared to controls (37.36% vs. 21.86%, respectively, p<0.0001, adjusted OR 2.13 (1.56-2.90)), as well as double deletions (15.38% vs. 10.38%, respectively, p<0.05). The carriers of GSTM1 deletion had significantly earlier onset of MS compared to the wild-type carriers (28.31 ± 8.45 vs. 30.64 ± 9.30 years, respectively, p = 0.03). CONCLUSION: This study suggests the potential pathogenic role of GSTT1 deletion on MS susceptibility. There are no similar data published so far, yet this study should be replicated in other populations.
BACKGROUND:Multiple sclerosis (MS) occurs as a result of interaction between genetic and environmental factors. Recent data support the view that oxidative damage is one of an early event in MS tissue injury. The safe elimination of reactive oxygen species and toxins via glutathione S-transferase (GST) pathways is required in order to protect cells against reactive oxygen-induced damage. The aim of our study was to analyze the possible association of GSTM1 and GSTT1 gene polymorphisms with the susceptibility and clinical parameters of MS, in 455 consecutive patients and 366 controls. METHODS: A multiplex polymerase chain reaction (PCR) was used to detect the deletions in GSTM1 and GSTT1 genes. RESULTS:Patients with MS had significantly higher frequency of GSTT1 null genotype compared to controls (37.36% vs. 21.86%, respectively, p<0.0001, adjusted OR 2.13 (1.56-2.90)), as well as double deletions (15.38% vs. 10.38%, respectively, p<0.05). The carriers of GSTM1 deletion had significantly earlier onset of MS compared to the wild-type carriers (28.31 ± 8.45 vs. 30.64 ± 9.30 years, respectively, p = 0.03). CONCLUSION: This study suggests the potential pathogenic role of GSTT1 deletion on MS susceptibility. There are no similar data published so far, yet this study should be replicated in other populations.
Authors: José A G Agúndez; Elena García-Martín; Carmen Martínez; Julián Benito-León; Jorge Millán-Pascual; María Díaz-Sánchez; Patricia Calleja; Diana Pisa; Laura Turpín-Fenoll; Hortensia Alonso-Navarro; Lucía Ayuso-Peralta; Dolores Torrecillas; Esteban García-Albea; José Francisco Plaza-Nieto; Félix Javier Jiménez-Jiménez Journal: Cell Mol Immunol Date: 2014-12-22 Impact factor: 11.530
Authors: Mehdi Aliomrani; Mohammad A Sahraian; Hamid Shirkhanloo; Mohammad Sharifzadeh; Mohammad R Khoshayand; Mohammad H Ghahremani Journal: Neurol Sci Date: 2017-04-21 Impact factor: 3.307
Authors: Amrita Singh; Kashi N Prasad; Aloukick K Singh; Satyendra K Singh; Kamlesh K Gupta; Vimal K Paliwal; Chandra M Pandey; Rakesh K Gupta Journal: Mol Neurobiol Date: 2016-03-28 Impact factor: 5.590