Ultrastructural changes of ganglionic and M?ller’s cells of the rat’s retina caused by methanol intoxication
DOI:
https://doi.org/10.31288/oftalmolzh20151123127Keywords:
Retina, ganglionic cells, processes of M?ller’s cells, ultrastructure, methanolAbstract
Introduction. Methyl alcohol (methanol) is a strong toxic substance, which is used in varnish-and-paint industry, at the petrol stations, etc that increases the possibility of its incidental or chronic influence on the human organism. According to the clinical and experimental data methanol primarily damage the optic nerve, retina and the brain tissues. Therefore, it is important to study mechanisms of the damaging effect of methanol on live tissues, namely, the retina of the experimental animal deeper at the subcellular level.
Objective. Electronic-microscopic study of changes of the ganglionic cells (GC) and processes of M?ller’s cells (PMC) that surround GC of the retina of white rats in dynamics (1–14 days) after single intraabdominal introduction of methanol in the dose of 2.5 g/kg of the body mass.
Material and methods. The work was done on 18 white Wistar’s rats of 250–300 g of weight, which were subdivided into two groups: 1- a group under study where the rats were given single injection of methanol in the dose of 2.5 f/kg of the body mass. II — a group with control animals, which were introduced a physiological solution in the same volume. There was investigated the ultrastructure of GC and PMC of the rats’ retina in 1, 3, 7 and 14 days after introduction of methanol in the electronic microscope PEM-100–01.
Results. It is shown that methanol caused primary and considerable damage of GC of the retina. The cells of small and middle size were the most vulnerable of GC. During the follow-up investigation destructive changes increased both on GC and PMC. It was found that mitochondria were the most vulnerable structures to the damage resulting in significant energy dysfunction of the cells. Parallel to the destruction signs there were signs of increased protein-synthesized activity in GC, which was a manifestation of compensation-restoration processes in them.
References
1.Bitenskii VS. The role of alcohol and drug abuse in the demographic crisis in Ukraine. Zhurn. AMN Ukrainy. 2007;3:543-50. In Russian.
2.Dumbrova N. E., Molchanyuk N. I. Ultrastructural changes in the elements of the choroids-retinal complex of the eyes of rats after the action of the methyl alcohol. Oftalmol Zh. 2009;5:54-7. Russian. https://doi.org/10.31288/oftalmolzh200955457
3.Dumbrova N. E., Molchanyuk N. I. Influence of methanol on ultrasound structure of retinal neural cells in the rat's eye. Zhurn. AMN Ukrainy. 2010;16(3):507-14. In Russian.
4.Serov VV, Zabrodskii PF, Kirichuk VF. Effect of acute methanol poisoning on lipid peroxidation and corticosterone concentration in blood. Vestn. Novykh med. Tekhnologii. 2007;14(1):81. In Russian.
5.Shulpina NB, Rozhnov VE, Galiaskarova FR. Alcohol intoxication and organ of vision. Vestn Oftalmol. 1987;1:62-5. In Russian.
6.Tsymbalyuk VI, Nosov AT, Chebatoreva LL, Vasyuta VA. Electrophysiological and morphological parameters, the state of the visual analyzer in the dynamics of the use of trofin in methanol intoxication. Ukr. Neirikhirurgich. Zhurnal. 2004;3:97-102. In Russian.
7.Nicholls P. Formate as an inhibitor of cytochrome c oxidase. Biochem Biophys Res Commun. 1975;67:610-6.https://doi.org/10.1016/0006-291X(75)90856-6
8.Treichel JL, Murray TG, Burton TC et all. Retinal toxicity in methanol poisoning. Retina. 2004;24:309-12.https://doi.org/10.1097/00006982-200404000-00023
9.Rajamani R, Muthuvel A, Senthilvelan M, Sheeladevi R. Oxidative stress induced by methotrexate alone and in the presence of methanol in discrete regions of the rodent brain, retina and optic nerve. Toxicol. Lett. 2006;12(5):12-5.
Downloads
Published
How to Cite
Issue
Section
License
Copyright (c) 2026 Н. Е. Думброва, Н. И. Молчанюк

This work is licensed under a Creative Commons Attribution 4.0 International License.
This work is licensed under a Creative Commons Attribution 4.0 International (CC BY 4.0) that allows users to read, download, copy, distribute, print, search, or link to the full texts of the articles, or use them for any other lawful purpose, without asking prior permission from the publisher or the author as long as they cite the source.
COPYRIGHT NOTICE
Authors who publish in this journal agree to the following terms:
- Authors hold copyright immediately after publication of their works and retain publishing rights without any restrictions.
- The copyright commencement date complies the publication date of the issue, where the article is included in.
DEPOSIT POLICY
- Authors are permitted and encouraged to post their work online (e.g., in institutional repositories or on their website) during the editorial process, as it can lead to productive exchanges, as well as earlier and greater citation of published work.
- Authors are able to enter into separate, additional contractual arrangements for the non-exclusive distribution of the journal's published version of the work with an acknowledgement of its initial publication in this journal.
- Post-print (post-refereeing manuscript version) and publisher's PDF-version self-archiving is allowed.
- Archiving the pre-print (pre-refereeing manuscript version) not allowed.








