Neuromuscular Functions on Experimental Acute Methanol Intoxication

Abstract

Objective: The incidence of accidental or suicidal ingestion of methyl alcohol is high and methyl alcohol intoxication has high mortality. Methyl alcohol intoxication causes severe neurological sequelae and appears to be a significant problem. Methyl alcohol causes acute metabolic acidosis, optic neuropathy leading to permanent blindness, respiratory failure, circulatory failure and death. It is metabolised in the liver, and its metabolite formic acid has direct toxic effects, causing oxidative stress, mitochondrial damage and increased lipid peroxidation associated with the mechanism of neurotoxicity. Methanol is known to cause acute toxicity of the central nervous system; however, the effects on peripheral neuromuscular transmission are unknown. In our study, we aimed to investigate the electrophysiological effects of experimentally induced acute methanol intoxication on neuromuscular transmission in the early period (first 24 h). Methods:After approval by the Animal Experiment Ethics Committee of Ege University, the study was carried out on 10 Wistar rats, each weighing about 200 g. During electrophysiological recordings and orogastric tube insertion, the rats were anaesthetised using intra-peritoneal (IP) injection of ketamine 100 mg kg −1 and IP injection of xylazine 10 mg kg −1 . The rats were given 3 g kg −1 methyl alcohol by the orogastric tube. Electrophysiological measurements from the gastrocnemius muscle were compared with baseline.Results: Latency measurements before and 24 h after methanol injection were 0.81±0.11 ms and 0.76±0.12 ms, respectively. CMAP amplitude measurements before and 24 h after methanol injection were 9.85±0.98 mV and 9.99±0.40 mV, respectively. CMAP duration measurements before and 24 h after methanol injection were 9.86±0.03 ms and 9.86±0.045 ms, respectively. Conclusion:It was concluded that experimental methanol intoxication in the acute phase (first 24 h) did not affect neuromuscular function.

Exercise Regulates the Metabolic Homeostasis of Methamphetamine Dependence

“…Our data suggested that METH might stimulate glyoxylate and dicarboxylate metabolism with significantly increased levels of glyceric acid, cis-aconitic acid, citric acid, isocitric acid, glycolic acid, succinic acid, oxalic acid, and formic acid. As the end product of the glyoxylate and dicarboxylate metabolism pathway, formic acid has direct toxic effects that can cause oxidative stress, mitochondrial damage, and increased lipid peroxidation associated with the mechanism of neurotoxicity [ 24 ]. The classical mechanism of METH neurotoxicity is that METH causes oxidative stress in neurons by increasing release and reuptake blockage that then leads to excessive cytoplasmic dopamine [ 25 ].…”

1-Boc-Piperidine-4-Carboxaldehyde Prevents Binge-Eating Behaviour and Anxiety in Rats

“…It is important to highlight that as the volume of injection for treatments was 1 mL kg −1 i.p., the total amount of methanol that rats received was around 20 µg 3 times a week. Note that although methanol is a vehicle that may raise some concerns because of its capacity for exerting deleterious effects, the toxic doses in rodents are more than 2000 times higher [43, 44] than the total amount used in the present study (e.g., LD50 in rats = 9.5 g/kg) [45].…”

Methanol-induced optic neuropathy: a still-present problem

“…Previous animal studies have shown that methanol intoxication can affect the function of the neuroimmune system and induce both specific and non-specific systemic immune responses, probably mainly by increasing oxidative stress and secondary changes in corticosterone levels resulting from dysfunction of the hypothalamic–pituitary axis (Moral et al 2015 ; Parthasarathy et al 2006 , 2007 ). Examination of the optic nerve tissue of rats treated with the combination of methotrexate (MTX) and methanol showed higher expression of the final DNA degeneration product—8-hydroxy-2'-deoxyguanosine (8-OHdG), as well as molecules involved in the inflammatory response such as tumor necrosis factor-alpha (TNF-α), nuclear factor-kappa β (NF-kβ), and interleukin 1 beta (IL-1β), which suggests 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 (Taşlı et al 2018 ).…”