Research Article

GSTM1 polymorphism in patients with primary open-angle glaucoma

Published: September 13, 2012
Genet. Mol. Res. 11 (3) : 3256-3262 DOI: https://doi.org/10.4238/2012.September.12.8
Cite this Article:
A.M. Barbosa, A.B. Frare, N.B. Costa, R.E. Silva, K.K.V.O. Moura (2012). GSTM1 polymorphism in patients with primary open-angle glaucoma. Genet. Mol. Res. 11(3): 3256-3262. https://doi.org/10.4238/2012.September.12.8
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Abstract

Primary open-angle glaucoma (POAG) is characterized by loss of retinal ganglion cells, optic nerve damage and irreversible loss of visual field. Glaucoma is the second leading cause of blindness worldwide. It was estimated that in 2010 there were about 60.5 million glaucoma cases worldwide; among these patients, 4.5 million will become bilaterally blind. Glutathione S-transferases (GST) are a group of drug-metabolizing enzymes of phase-II that act in the detoxification of xenobiotics and inactivate end-products formed as secondary metabolites during oxidative stress. Through PCR amplification, we analyzed the GSTM1 gene in DNA samples from 25 patients with POAG and 25 controls; 14 of the patients presented the GSTM1 gene null polymorphism while only eight of the control group had this gene.Although the POAG patients had a higher frequency of GSTM1, the difference was not significant (P = 0.0874); this lack of significance could be due to the small sample size.

Primary open-angle glaucoma (POAG) is characterized by loss of retinal ganglion cells, optic nerve damage and irreversible loss of visual field. Glaucoma is the second leading cause of blindness worldwide. It was estimated that in 2010 there were about 60.5 million glaucoma cases worldwide; among these patients, 4.5 million will become bilaterally blind. Glutathione S-transferases (GST) are a group of drug-metabolizing enzymes of phase-II that act in the detoxification of xenobiotics and inactivate end-products formed as secondary metabolites during oxidative stress. Through PCR amplification, we analyzed the GSTM1 gene in DNA samples from 25 patients with POAG and 25 controls; 14 of the patients presented the GSTM1 gene null polymorphism while only eight of the control group had this gene.Although the POAG patients had a higher frequency of GSTM1, the difference was not significant (P = 0.0874); this lack of significance could be due to the small sample size.