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Related Experiment Videos

Miroslav Stamenkovic1,2, Vesna Lukic1, Sonja Suvakov3,4

  • 1University Eye Clinic, Medical Center Zvezdara, Belgrade 11000, Serbia.

International Journal of Ophthalmology
|September 19, 2018
PubMed
Summary

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Glutathione transferase theta 1 (GSTT1)-active genotype increases primary open angle glaucoma (POAG) risk, especially when combined with GSTM1-null genotype or environmental factors like smoking. These findings suggest gene-environment interactions in POAG development.

Area of Science:

  • Genetics
  • Ophthalmology
  • Environmental Health

Background:

  • Glutathione transferase (GST) enzymes play a role in detoxification.
  • Genetic polymorphisms in GST genes, such as GSTT1 and GSTM1, may influence susceptibility to diseases.
  • Primary open-angle glaucoma (POAG) is a complex optic neuropathy with multifactorial etiology.

Purpose of the Study:

  • To investigate the association between GSTT1 and GSTM1 gene polymorphisms and POAG risk.
  • To explore the combined effects of these polymorphisms with environmental risk factors (smoking, hypertension, diabetes) on POAG development.

Main Methods:

  • A case-control study involving 102 POAG patients and 202 controls.
  • Multiplex-polymerase chain reaction was used to determine GSTT1 and GSTM1 genotypes.
Keywords:
GSTM1GSTT1diabetes mellitushypertensionprimary open angle glaucoma risksmoking

Related Experiment Videos

  • Logistic regression analysis was employed to assess disease risk.

    • Main Results:

    • GSTM1-null genotype alone did not significantly increase POAG risk.
    • GSTT1-active genotype was associated with a nearly two-fold increased POAG risk.
    • The combination of GSTT1-active and GSTM1-null genotypes further elevated POAG risk (OR=4.36).
    • GSTT1-active genotype showed significantly increased POAG risk when combined with smoking, hypertension, or diabetes.

    Conclusions:

    • Both GSTM1-null and GSTT1-active genotypes are linked to elevated POAG risk, particularly in smokers.
    • These findings highlight a potential gene-environment interaction in the pathogenesis of POAG.
    • GST polymorphisms may modify an individual's susceptibility to POAG in the presence of specific environmental exposures.