“…38 Similarly, in a methanol-induced optic neurite study, it was found that taxifolin reduced the release of NF-κ B and TNF-α. 39 After evaluating all the data, we concluded that taxifolin had an antioxidant and antiinflammatory effect on the brain damage induced by acrylamide.…”
“…38 Similarly, in a methanol-induced optic neurite study, it was found that taxifolin reduced the release of NF-κ B and TNF-α. 39 After evaluating all the data, we concluded that taxifolin had an antioxidant and antiinflammatory effect on the brain damage induced by acrylamide.…”
“…2 ) (Masoud et al 2016 ). In addition, recent investigations suggest that the inflammatory background also plays an important role in the development of pathophysiological changes in the eye tissues caused by the methanol and its metabolites (Ahiskali et al 2019 ; Taşlı et al 2018 ). Fig.…”
“…Primates, including humans, in contrast to non-primates, are sensitive to methanol due to the limited ability to rapidly metabolize and eliminate methanol and its metabolites from the body (Eells et al 2000 ; Plaziac et al 2003 ). Formic acid inhibits oxidative phosphorylation by binding to a key enzyme in the mitochondrial respiratory chain—cytochrome c oxidase—causing intracellular adenosine triphosphate (ATP) deficiency (Ahiskali et al 2019 ; Saoudi et al 2011 ). This effect was observed in both in vitro and in vivo studies at the concentration of formic acid ranging from 5 to 30 nM (Treichel et al 2003 ).…”
Methanol-induced optic neuropathy (Me-ION) is a serious condition that may result in long-term or irreversible visual impairment or even blindness secondary to damage and loss of function of the optic nerve and retina. Me-ION shows a tendency to occur as mass poisonings around the world with a clear predilection for poor societies in developing countries. The main mechanism underlying the molecular basis of Me-ION is the inhibition of the mitochondrial oxidative phosphorylation process through the binding of the toxic metabolite of methanol—formic acid—with the key enzyme of this process—cytochrome c oxidase. However, other mechanisms, including damage to the eye tissues by oxidative stress causing the intensification of the oxidative peroxidation process with the formation of cytotoxic compounds, as well as an increase in the synthesis of pro-inflammatory cytokines and influence on the expression of key proteins responsible for maintaining cell homeostasis, also play an important role in the pathogenesis of Me-ION. Histopathological changes in the eye tissues are mainly manifested as the degeneration of axons and glial cells of the optic nerve, often with accompanying damage of the retina that may involve all its layers. Despite the development of therapeutic approaches, persistent visual sequelae are seen in 30–40% of survivors. Thus, Me-ION continues to be an important problem for healthcare systems worldwide.
“…According to clinical data [21,24,27] in acute methanol poisoning there is optic nerve neuropathy. Studies in rats have shown that methanol poisoning in ON damages nerve fibers (NF), disrupts axoplasmic circulation due to blockade of energy-producing processes associated with mitochondrial pathology [1,7,20,22]. We previously found that a single intra-abdominal injection of rats 100% methanol at a dose of 0.75 g/kg body weight, which is 10 part of the lethal dose, causes in ON, primarily changes in the myelin sheaths of nerve fibers of large caliber already in the first hours of observation [6].…”
There are, quite often, cases of poisoning of human population with poor-quality alcoholic drinks, which include methanol. The optic nerve, retina and brain tissues are initially affected. A long-term study aimed at identifying initial structural changes in the visual analyzer in the application of various doses of methanol and its mixture with ethanol was carried out. Purpose: to study the dynamics of ultrastructural changes in glial cells and nerve fibers of the optic nerve, which are caused by mixture of ethanol 40% and methanol 100% in a ratio of 3:1 with a dose of methanol of 0.75 g/kg of rat weight. We examined the ultrastructure of the orbit part of the optic nerve of 43 adult rats (Wistar line) in the period from 3 hours to 14 days after one-time intra-abdominal injection of ethanol 40% and methanol 100%, 100% methanol, the dose of methanol is 0.75 g/kg of rat weight. In rats, LD50 is 9.5 g/kg of their weight. It was found out, that within 3 hours after the injection of the mixture of alcohols, the myelin sheath of large-caliber nerve fibers exfoliated, the axoplasm swelled and the mitochondria in their axons pathologically changed, the mitochondria altered in glial cells, which influenced the quality of nerve impulses and axoplasmic transport of substances. In the dynamics of the study, alterative changes in structures of the optic nerve progressed with the complete destruction of part of glial cells by 7 days, mainly in the first 3 days. After the use of methanol 100%, changes in structures of the optic nerve were similar to changes in them after the use of a mixture of alcohols, but with more significant pathology at all periods of observation with the peak of their manifestation on the 7th day. In glial cells and axons of nerve fibers from the 1st day of the study, signs of compensatory and restorative processes were found: they increased protein-synthesizing and energy-forming functions that were aimed at restoring the damaged ultrastructure. It is established, that 3 hours after the injection of a mixture of alcohols, reactive changes in the structures of the optic nerve of rats took place, which from the 1st day develop into pathological changes and are observed up to 14 days with the peak of their activity on the 7th day of the study. After the use of methanol 100%, the ultrastructure of the optic nerve of rats is more damaged than after the injection of a mixture of alcohols. It is proved, that methanol has a leading place in the development of pathological changes in structures of the optic nerve after the injection of a mixture of alcohols.
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