Association of neuroretina destruction markers with retinal level of hydrogen sulfide in traumatic injury of the visual analyzer
DOI:
https://doi.org/10.11603/mcch.2410-681X.2018.v0.i2.9144Keywords:
visual analyzer, contusion, hydrogen sulfide, neuroretinal destruction.Abstract
Introduction. Glutamate exitotoxicity plays a leading role in damaging of the visual analyzer of traumatic genesis. As it was shown recently, hydrogen sulfide (H2S) system is involved in the regulation of neurotransmission, ophthalmotonus and retinal injury, but its role in the pathogenesis of post-traumatic injury of the visual analyzer has not been clarified.
The aim of the study – to evaluate the association of neuroretinal destruction markers with retinal level of hydrogen sulfide in experimental traumatic injury of the visual analyzer.
Research Methods. Experiments were carried out on 24 male rabbits weighing 3.0–3.9 kg. Traumatic injury of visual analyzer in rabbits was caused by the action of carbon dioxide stream under pressure on the cornea of the eye. The levels of H2S, glutamate, cytometric markers of apoptosis in the retina, and the levels of neuron specific enolase (NSE) and S100 protein in the blood serum were determined.
Results and Discussion. Traumatic injury of the visual analyzer in the rabbits was characterized by increase levels of NSE neuronal markers and S100 protein in serum, and increase in glutamate level and the number of cells in the SUB-G0G1 phase (apoptotic marker) in the retina during 24 hours, followed by the escalation of neuroretinodestruction signs in 7 days. After 24 hours after the injury, increase of H2S level (2-times) was observed in retina, but in 7 days its level was significantly decreased (4-times). Formation of H2S deficiency in retina was associated with aggravation of glutamate excitotoxicity and neuroretinal destruction signs.
Conclusions. Thus, H2S system is involved in the mechanisms of retina injury in case of contusive eye trauma. H2S level correction in the retina may be a promising strategy in traumatic injury to the visual analyzer and this direction is appropriate for further study.
References
GBD 2016 Disease and Injury Incidence and Prevalence Collaborators (2017). Global, regional, and national incidence, prevalence, and years lived with disability for 328 diseases and injuries for 195 countries, 1990–2016: a systematic analysis for the Global Burden of Disease Study 2016. Lancet, 390 (10100), 1211-1259. http://doi.org/10.1016/S0140-6736(17)32154-2
Kuhn, F., Morris, R., Witherspoon, C.D., & Mann, L. (2006). Epidemiology of blinding trauma in the United States Eye Injury Registry. Ophthalmic Epidemiol., 13 (3), 209-216.
Onose, G., Daia-Chendreanu, C., Haras, M., Ciurea, A.V., & Anghelescu, A. (2011). Traumatic brain injury: Current endeavours and trends for neuroprotection and related recovery. Romanian Neurosurgery, 18 (1),
-30.
Ullian, E.M., Barkis, W.B., Chen, S., Diamond, J.S., & Barres, B.A. (2004). Invulnerability of retinal ganglion cells to NMDA excitotoxicity. Mol. Cell Neurosci, 26 (4), 544-557.
Du, J., Jin, H., & Yang, L. (2017). Role of Hydrogen Sulfide in Retinal Diseases. Frontiers in Pharmacology, 8, 588. http://doi.org/10.3389/fphar.2017.00588
Huang, S., Huang, P., Liu, X., Lin, Z., Wang, J., Xu, S., Guo, L., Leung, C.K., & Zhong, Y. (2017). Relevant variations and neuroprotecive effect of hydrogen sulfide in a rat glaucoma model. Neuroscience, 341, 27-41. doi:
1016/j.neuroscience.2016.11.019.
Gersztenkorn, D., Coletta, C., Zhu, S., Ha, Y., Liu, H., Tie, H., Zhou, J., … & Motamedi M. (2016). Hydrogen sulfide contributes to retinal neovascularization
in ischemia-induced retinopathy. Invest. Ophthalmol. Vis. Sci., 57(7), 3002-3009. doi: 10.1167/iovs.15-18555.
Chereshniuk, I.L., Komnatska, K.M., Povkh, V.L., & Khodakivskyi, O.A. (2016). Patent na korysnu model 109789 Ukraina, MPK A61F 9/0. Sposib modeliuvannia kontuzii oka dlia skryninhovoi otsinky neiroretynoprotektyvnoi
aktyvnosti likarskykh zasobiv ta biolohichno aktyvnykh rechovyn [Patent for Utility Model No109789 UA]. Kyiv, Ukraine: Ukrainian Intellectual Property Institute [in Ukrainian].
Wiliński, B., Wiliński, J., Somogyi, E., Piotrowska, J., & Opoka, W. (2013) Metformin raises hydrogen sulfide tissue concentrations in various mouse organs. Pharmacol Rep., 65 (3), 737-742.
Popova, L.D. (2006) Vplyv kinurenovoi kysloty na vmist zbudzhuvalnykh i halmivnykh mediatoriv u shchuriv iz riznym rivnem sudomnoi hotovnosti [Effect of kynurenic acid on the content of excitatory and inhibitory mediators in rats with different levels of seizure readiness]. Ukrainskyi biokhimichnyi zhurnal – Ukrainian Biochemical Journal, 78 (5), 120-126 [in Ukrainian].
Kochetov, G.A. (1980) Prakticheskoe rukovodstvo po enzimologii [Practical guide to enzymology]. Moscow: Vysshaya shkola [in Russian].
Zaichko, N.V., Melnik, A.V., Yoltukhivskyy, M.M., Olhovskiy, A.S., & Palamarchuk, I.V. (2014) Hydrogen sulfide: modern aspects of metabolism, biological and medical role. Ukr. Biochem. J., 86 (5), 5-25.
Zhang, J.Y., Ding, Y.P., Wang, Z., Kong, Y., Gao, R., & Chen, G. (2017) Hydrogen sulfide therapy in brain diseases: from bench to bedside. Med. Gas. Res., 7(2), 113-119. doi: 10.4103/2045-9912.208517
Kimura, Y., Goto, Y.I., & Kimura H. (2010) Hydrogen sulphide increases glutathione production and suppresses oxidative stress in mitochondria. Antioxidants and Redox Signaling, 12 (1), 1-13.
