scholarly journals N-acetylcysteine relieves neurologic signs of acute ethanol hangover in rats

2021 ◽  
Vol 7 (1) ◽  
pp. 75-83
Author(s):  
Denis V. Kurkin ◽  
Evgeny I. Morkovin ◽  
Nazar A. Osadchenko ◽  
Dmitry A. Bakulin ◽  
Marina A. Dubrovina ◽  
...  
Keyword(s):  
Motor Skills ◽  
Water Maze ◽  
Alcohol Intoxication ◽  
Cognitive Impairments ◽  
Morris Water Maze Test ◽  
Fine Motor ◽  
Ethanol Intoxication ◽  
Maze Test ◽  
Acute Ethanol ◽  
Acute Ethanol Intoxication

Introduction: Alcohol abuse is one of the grave social and medical problems in many countries, including Russia. Alcohol not only negatively affects health, social and family relationships, but also a person’s performance. Hangover, which is a one of the negative consequences of alcohol intake, is a complex of neurological and somatic symptoms that occur when ethanol is almost completely metabolized to acetaldehyde. This condition, despite the severity and potential economic damage, remains poorly understood, and there are no effective medicines to treat it. Aim: to provide an experimental basis for the possibility of using N-acetylcysteine (NAC), a precursor of glutathione, as a medicine for prevention of the neurological and cognitive impairments due to alcohol intoxication. Materials and Methods: The study used male Wistar rats, which were intraperitoneally injected with ethanol at a dose of 3 g/kg to simulate acute ethanol intoxication. Sixty minutes before the injection, the animals from the experimental groups were gavaged with NAC (1 g/kg) or with an equivalent volume of saline. Immediately after awakening and 3 h after it, the animals were assessed for neurological deficits, motor skills, spontaneous motor activity, and cognitive functions. After the completion of the behavioral tests, the animals were euthanized to assess the level of glutathione, triglycerides (TGs), and malonic dialdehyde (MDA) in liver homogenates, and to determine the activity of enzymatic antioxidant systems and serum aminotransferases. Results and Discussion: The ethanol intoxication in the animals from the control group was associated with pronounced signs of neurological and cognitive impairments, including low spontaneous motor and exploratory activity, impaired fine motor skills in the adhesive test, and cognitive function decline in the Morris water maze test. The rats which had received NAC before ethanol injection demonstrated better fine motor skills in the adhesive test, a higher level of spontaneous motor activity and better performance in the Morris water maze test (in comparison to the animals treated with saline before alcohol intoxication). In the animals which had received NAC, the levels of glutathione, MDA, and TGs, as well as the activity of liver antioxidant enzymes, were closer to the values of the intact rats to a greater extent than in the animals that had been injected with ethanol and received saline. Conclusion: Orally administered NAC before acute ethanol intoxication led to a decrease in the severity of neurological deficiency in rats and reduced the amnesic effect of ethanol. This could be due to an improvement of ethanol metabolism and a decrease in the severity of disorders associated with oxidative stress and liver dysfunction.

scholarly journals The effect of sorbents on the serum levels of copper, iron and their transporting proteins at alcohol intoxication

2015 ◽  
Vol 96 (5) ◽  
pp. 868-871
Author(s):  
N A Terekhina ◽  
E V Zhidko ◽  
G A Terekhin ◽  
A G Orbidans
Keyword(s):  
Alcohol Abuse ◽  
Membrane Permeability ◽  
Erythrocyte Membrane ◽  
Alcohol Intoxication ◽  
Serum Levels ◽  
Ethanol Intoxication ◽  
Ceruloplasmin Level ◽  
Acute Ethanol ◽  
Acute Ethanol Intoxication ◽  
Erythrocyte Membrane Permeability

Aim. Evaluate the effect of sorbents on erythrocyte membrane permeability and serum levels of copper, iron and their transporting proteins at acute ethanol intoxication. Methods. The study was performed on 94 rats. Acute alcohol intoxication was simulated on intact animals and in animals with prior artificial alcohol abuse. Acute ethanol intoxication was caused by intragastric administration of 40% ethanol at a dose of 0.5 of median lethal dose. Polysorb, Litovit, and Sapropel sorbents were administered at a dose of 3000 mg/kg 30 minutes after ethanol administration. permeability of erythrocyte membrane, serum levels of copper, iron, ceruloplasmin and transferrin were measured by spectrophotometry. Results. Levels of copper and iron in rat serum and erythrocyte membrane permeability significantly dropped compared to the control level at acute ethanol intoxication, ceruloplasmin level raised by 1.5 times, transferrin level did not change significantly. At acute ethanol intoxication in animals with prior artificial alcohol abuse, copper and iron levels and erythrocyte membrane permeability remained low, ceruloplasmin level remained high, transferrin level was decreased for 2 times. All sorbents were able to compensate the serum levels of copper, iron and ceruloplasmin in animals with prior artificial alcohol abuse, and Litovit and Polysorb also influenced on transferrin level. Conclusion. Compensatory effect of Polysorb, Litovit, and Sapropel on the serum levels of ceruloplasmin, copper, iron and transferrin and on erythrocyte membrane permeability was discovered at acute ethanol intoxication in animals with prior artificial alcohol abuse.

scholarly journals Acute ethanol intoxication induces preferred loss of presynaptic boutons devoid of mitochondria in vivo

2019 ◽  
Author(s):  
Jil Protzmann ◽  
Astha Jaiswal ◽  
Karl Rohr ◽  
Thomas Kuner ◽  
Sidney Cambridge ◽  
...  
Keyword(s):  
Alcohol Intoxication ◽  
Blood Alcohol Concentration ◽  
Memory Loss ◽  
Ethanol Exposure ◽  
Dense Core Vesicle ◽  
Ethanol Intoxication ◽  
Acute Ethanol ◽  
Presynaptic Boutons ◽  
Acute Ethanol Intoxication

AbstractAcute alcohol intoxication is frequently observed in modern societies and carries a vast burden, ranging from traffic accidents to transient memory loss. Despite years of intense research, the effects of acute ethanol intoxication on brain function remain incompletely understood. Here, we studied the effect of acute ethanol intoxication on axonal organelle trafficking and presynaptic structure using in vivo two photon microscopy in anesthetized mice. After a single intraperitoneal injection of ethanol, inducing a blood alcohol concentration of roughly 250 mg/dl, the axonal mitochondrial mobility was doubled while dense core vesicle mobility remained unaffected. Simultaneously imaging mitochondria and presynaptic boutons revealed that unoccupied presynaptic boutons perished more frequently after ethanol exposure, while boutons stably occupied with mitochondria mostly persisted. Our results define a novel mechanism of ethanol action and may explain difficulties in permanently storing new memories after episodes of intense ethanol consumption with a loss of synapses.

scholarly journals Acute and chronic ethanol consumption differentially impact pathways limiting hepatic protein synthesis

2008 ◽  
Vol 295 (1) ◽  
pp. E3-E9 ◽  
Author(s):  
Anne M. Karinch ◽  
Jonathan H. Martin ◽  
Thomas C. Vary
Keyword(s):  
Protein Synthesis ◽  
Alcohol Intoxication ◽  
Ethanol Consumption ◽  
Chronic Alcohol ◽  
Ethanol Intoxication ◽  
Initiation Factors ◽  
Eif2α Phosphorylation ◽  
Acute Ethanol ◽  
Acute Ethanol Intoxication ◽  
Hepatic Protein Synthesis

This review identifies the various pathways responsible for modulating hepatic protein synthesis following acute and chronic alcohol intoxication and describes the mechanism(s) responsible for these changes. Alcohol intoxication induces a defect in global protein synthetic rates that is localized to impaired translation of mRNA at the level of peptide-chain initiation. Translation initiation is regulated at two steps: formation of the 43S preinitiation complex [controlled by eukaryotic initiation factors 2 (eIF2) and 2B (eIF2B)] and the binding of mRNA to the 40S ribosome (controlled by the eIF4F complex). To date, alcohol-induced alterations in eIF2 and eIF2B content and activity are best investigated. Ethanol decreases eIF2B activity when ingested either acutely or chronically. The reduced eIF2B activity most likely is a consequence of twofold increased phosphorylation of the α-subunit of eIF2 on Ser51 following acute intoxication. The increase in eIF2α phosphorylation after chronic alcohol consumption is the same as that induced by acute ethanol intoxication, and protein synthesis is not further reduced by long-term alcohol ingestion despite additional reduced expression of initiation factors and elongation factors. eIF2α phosphorylation alone appears sufficient to maximally inhibit hepatic protein synthesis. Indeed, pretreatment with Salubrinal, an inhibitor of eIF2α(P) phosphatase, before ethanol treatment does not further inhibit protein synthesis or increase eIF2α phosphorylation, suggesting that acute ethanol intoxication causes maximal eIF2α phosphorylation elevation and hepatic protein synthesis inhibition. Ethanol-induced inhibition of hepatic protein synthesis is not rapidly reversed by cessation of ethanol consumption. In conclusion, sustained eIF2α phosphorylation is a hallmark of excessive alcohol intake leading to inhibition of protein synthesis. Enhanced phosphorylation of eIF2α represents a unique response of liver to alcohol intoxication, because the ethanol-induced elevation of eIF2α(P) is not observed in skeletal muscle or heart.

EFFECT OF POLYMORPHISM OF THE GABRA2 GENE ON THE DEGREE OF RAT POISONING IN ACUTE ETHANOL INTOXICATION

2019 ◽  
pp. 3-7
Author(s):  
N. S. Osechkina ◽  
G. V. Nazarov ◽  
M. B. Ivanov ◽  
E. G. Batotsyrenova ◽  
V. A. Kashuro ◽  
...  
Keyword(s):  
Genetic Markers ◽  
Inhibitory Action ◽  
Alcohol Intoxication ◽  
Biological Effects ◽  
Frequency Of Occurrence ◽  
Acute Alcohol Intoxication ◽  
Ethanol Intoxication ◽  
Acute Ethanol ◽  
Severe Intoxication ◽  
Acute Ethanol Intoxication

Four polymorphic GABRA2 gene variations: rs105733011, rs8168342, rs198286814, rs198837638 that can influence the formation of different biological effects of the organism when exposed to ethanol have been investigated. For rs105733011 polymorphism the frequency of occurrence of the CT genotype was found to be significantly higher (p < 0,05) among animals with «severe intoxication» – 37,0% than with «mild intoxication» – 14,0%. For rs198286814 polymorphism the tendency to the most frequent occurrence of the AG genotype in the group of animals with «severe intoxication» was established. Significant differences in the distribution of occurrence frequencies of the GG/AG genotypes in the studied groups for polymorphic loci rs8168342 and rs198837638 were not revealed. It was concluded that the rs105733011 polymorphism can be one of the genetic markers allowing to predict the degree of inhibitory action of ethanol in acute alcohol intoxication.

scholarly journals Heavy Ethanol Intoxication Increases Proinflammatory Cytokines and Aggravates Hemorrhagic Shock-Induced Organ Damage in Rats

2013 ◽  
Vol 2013 ◽  
pp. 1-9 ◽  
Author(s):  
Tsung-Ming Hu ◽  
Ru-Ping Lee ◽  
Chung-Jen Lee ◽  
Yi-Maun Subeq ◽  
Nien-Tsung Lin ◽  
...  
Keyword(s):  
Hemorrhagic Shock ◽  
Alcohol Intoxication ◽  
Lactic Dehydrogenase ◽  
Serum Levels ◽  
Organ Damage ◽  
Ethanol Intoxication ◽  
Total Blood ◽  
Cytokine Levels ◽  
Acute Ethanol ◽  
Acute Ethanol Intoxication

Hemorrhagic shock (HS) following acute alcohol intoxication can increase proinflammatory cytokine production and induce marked immunosuppression. We investigated the effects of ethanol on physiopathology and cytokine levels following HS in acutely alcohol-intoxicated rats. Rats received an intravenous injection of 5 g/kg ethanol over 3 h followed by HS induced by withdrawal of 40% of total blood volume from a femoral arterial catheter over 30 min. Mean arterial pressure (MAP) and heart rate (HR) were monitored continuously for 48 h after the start of blood withdrawal. Biochemical parameters, including hemoglobin, ethanol, glutamic oxaloacetic transaminase (GOT), glutamic pyruvic transaminase (GPT), blood urea nitrogen (BUN), creatinine (Cre), lactic dehydrogenase (LDH), and creatine phosphokinase (CPK), were measured at 30 min before induction of HS and 0, 1, 3, 6, 9, 12, 18, 24, and 48 h after HS. Serum tumor necrosis factor-α(TNF-α) and interleukin-6 (IL-6) levels were measured at 1 and 12 h after HS. The liver, kidneys, and lungs were removed for pathology at 48 h later. HS significantly increased HR, blood GOT, GPT, BUN, Cre, LDH, CPK, TNF-α, and IL-6 levels and decreased hemoglobin and MAP in rats. Acute ethanol intoxication further increased serum levels of GOT, GPT, BUN, Cre, LDH, CPK, TNF-αand IL-6 elevation following HS. Acutely intoxicated rats exacerbated the histopathologic changes in the liver, kidneys, and lungs following HS.

ECG changes in patients with acute ethanol intoxication

2007 ◽  
Vol 41 (2) ◽  
pp. 79-84 ◽  
Author(s):  
Willy Aasebø ◽  
Willy Aasebø ◽  
Jan Erikssen ◽  
Jørgen Jonsbu ◽  
Knut Stavem
Keyword(s):  
Ethanol Intoxication ◽  
Ecg Changes ◽  
Acute Ethanol ◽  
Acute Ethanol Intoxication

scholarly journals Musical Electroacupuncture May Be a Better Choice than Electroacupuncture in a Mouse Model of Alzheimer’s Disease

2016 ◽  
Vol 2016 ◽  
pp. 1-9 ◽  
Author(s):  
Jing Jiang ◽  
Gang Liu ◽  
Suhua Shi ◽  
Zhigang Li
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Mouse Model ◽  
Frontal Lobe ◽  
Morris Water Maze ◽  
Water Maze ◽  
Morris Water Maze Test ◽  
Maze Test ◽  
Model Of Alzheimer’S Disease ◽  
Samp8 Mice

Objectives. To compare musical electroacupuncture and electroacupuncture in a mouse model of Alzheimer’s disease.Methods. In this study, 7.5-month-old male senescence-accelerated mouse prone 8 (SAMP8) mice were used as an Alzheimer’s disease animal model. In the normal control paradigm, 7.5-month-old male SAMR1 mice were used as the blank control group (N group). After 15 days of treatment, using Morris water maze test, micro-PET, and immunohistochemistry, the differences among the musical electroacupuncture (MEA), electroacupuncture (EA), Alzheimer’s disease (AD), and normal (N) groups were assessed.Results. The Morris water maze test, micro-PET, and immunohistochemistry revealed that MEA and EA therapies could improve spatial learning and memory ability, glucose metabolism level in the brain, and Aβamyloid content in the frontal lobe, compared with the AD group (P<0.05). Moreover, MEA therapy performed better than EA treatment in decreasing amyloid-beta levels in the frontal lobe of mice with AD.Conclusion. MEA therapy may be superior to EA in treating Alzheimer’s disease as demonstrated in SAMP8 mice.

Protective Effects of Dendrobium nobile Lindl. Alkaloids on Alzheimer's Disease-like Symptoms Induced by High-methionine Diet

2021 ◽  
Vol 19 ◽  
Author(s):  
Tingting Pi ◽  
Guangping Lang ◽  
Bo Liu ◽  
Jingshan Shi
Keyword(s):  
Alzheimer’S Disease ◽  
Learning And Memory ◽  
Morris Water Maze ◽  
Water Maze ◽  
Cpg Island ◽  
Morris Water Maze Test ◽  
Dendrobium Nobile ◽  
Maze Test ◽  
Neuron Damage ◽  
Cpg Island Methylation

Background: High methionine-diet (HMD) causes Alzheimer's disease (AD)-like symptoms. Previous studies have shown that Dendrobium nobile Lindle. alkaloids (DNLA) had potential benefits for AD. Object: Whether DNLA can improve AD-like symptoms induced by HMD is to be explored. Method: Mice were fed with 2% HMD diet for 11 weeks, the DNLA20 control group (20 mg/kg), DNLA10 group (10 mg/kg), and DNLA20 group (20 mg/kg) were administrated with DNLA for 3 months. Morris water maze test was used to detect learning and memory ability. Neuron damage was evaluated by HE and Nissl stainings. Levels of homocysteine (Hcy), beta-amyloid 1-42 (Aβ1-42), S-adenosine methionine (SAM), and S-adenosine homocysteine (SAH) were detected by ELISA. Immunofluorescence and western blotting (WB) were used to determine the expression of proteins. CPG island methylation. Results: Morris water maze test revealed that DNLA improved learning and memory dysfunction. HE, Nissl, and immunofluorescence stainings showed that DNLA alleviated neuron damage and reduced the 5-methylcytosine (5-mC), Aβ1-40, and Aβ1-42 levels. DNLA also decreased the levels of Hcy and Aβ1-42 in the serum, along with decreased SAM/SAH levels in the liver tissue. WB results showed that DNLA down-regulated the expression of the amyloid-precursor protein (APP), presenilin-1 (PS1), beta-secretase-1 (BACE1), DNA methyltransferase1 (DNMT1), Aβ1-40, and Aβ1-42 proteins. DNLA also up-regulated the expression of the protein of insulin-degrading enzyme (IDE), neprilysin (NEP), DNMT3a, and DNMT3b. Meanwhile, DNLA increased CPG island methylation levels of APP and BACE1 genes. Conclusions: DNLA alleviated AD-like symptoms induced by HMD via the DNA methylation pathway.

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