Kazan medical journalKazan medical journal0368-48142587-9359Eco-Vector187410.17816/KMJ1874Research ArticleThe state of the oxidation-reduction system in patients with primary open angle glaucomaGazizovaI Rilmira_ufa@rambler.ruBashkir State Medical University, Ufa, Russia1506201293348849028032016Copyright © 2012, Gazizova I.R.2012Aim. To study the state of the oxidation-reduction system in patients with primary open-angle glaucoma. Methods. Conducted were biochemical studies of the state of the oxidation-reduction system in 30 patients with primary open-angle glaucoma. The level of lipid peroxidation of cell membranes was determined in blood serum by the method of accumulation of malondialdehyde based on its interaction with thiobarbituric acid. The state of the antioxidant system was assessed according to the activity of superoxide dismutase, catalase, glutathione reductase and the content of thiol disulfide groups in the blood. The concentration of lactate in the blood serum was determined using an automated analyzer. Results. In patients with a chronic course of glaucoma elevated levels of oxidized thiol groups of proteins, increased activity of antioxidant enzymes, activation of lipid peroxidation processes, increased lactate content have been identified. Conclusion. Changes in the oxidation-reduction system in patients with primary open-angle glaucoma may be a sign of mitochondrial dysfunction.primary open-angle glaucomathiol groups of proteinsantioxidant enzymeslipid peroxidationпервичная открытоугольная глаукоматиоловые группы белковферменты антиоксидантной защитыперекисное окисление липидов[Алексеев В.Н., Мартынова Е.Б., Малеванная О.А. и др. Значение митохондриальной патологии в медицине и в офтальмологии // Глаукома: теория и практика. Рос. глаукомная школа: Сб. научн. тр. - СПб.: Человек и его здоровье, 2011. - С. 3-5.][Волков В.В. Глаукома при псевдонормальном давлении: Руководство для врачей. - М.: Медицина, 2001. - 352 с.][Нестеров А.П. Первичная открытоугольная глаукома: патогенез и принципы лечения // Клин. офтальмология. - 2000. - №1. - С. 4-5.][Browne S.E., Beal M.F. The energetics of Huntington’s disease // Neurochem. Res. - 2004. - Vol. 29. - Р. 531-546.][Calandrella N., Scarsella G., Pescosolido N. et al. Degenerative and apoptotic events at retinal and optic nerve level after experimental induction of ocular hypertension // Mol. Cell. Biochem. - 2007. - Vol. 301 - Р. 155-163.][Carelli V., Ross-Cisneros F.N., Sadun A.A. Mitochondrial dysfunction as a cause of optic neuropathies // Prog. Retin. Eye Res. - 2004. - Vol. 23. - Р. 53-89.][Danesh-Meyer H.V. Neuroprotection in glaucoma: recent and future directions // Curr. Opin. Ophthal. - 2011. - Vol. 22. - P. 78-86.][George Y.X., Van Bergen N.J., Trounce I.A. et al. Mitochondrial Dysfunction and Glaucoma // J. Glaucoma. - 2009. - Vol. 18. - Р. 93-100.][Kujoth G.C., Hiona A., Pugh T.D. et al. Mitochondrial DNA mutations, oxidative stress, and apoptosis in mammalian aging // Science. - 2005. - Vol. 309. - Р. 481-484.][Schmiedel J., Jackson S., Schefer J., Reichmann H. Mitochondrial сytopathies // J. Neurol. - 2003. - Vol. 250. - P. 267-277.]