Similarly, Zn deficiency in lung epithelia and alveolar macrophages decreases lung barrier function resulting in respiratory distress syndrome. Zn deficiency in the gut results in increased gut permeability, ultimately leading to endotoxemia and systemic inflammation. It is demonstrated that alcohol-induced modulation of zinc transporters results in decreased Zn levels in lungs, liver, gut, and brain. The scholarly published articles on the association between Zn metabolism and alcohol-associated disorders (liver, brain, lung, gut dysfunction, and fetal alcohol syndrome) have been reviewed. To review data on the role of ethanol-induced alteration of Zn homeostasis in mediation of adverse effects of alcohol abuse. However, there were significant differences with regard to amount of alcohol and water consumed but not API, in all the treatment groups in post-hoc test.Conclusions: It is unclear on to the alcohol de-addiction potential of zinc as monotherapy and combination therapy with topiramate. Thirty male rats divided into five groups, each containing six rats were treated as control group, receiving 1ml/kg/d distilled water orally zinc sulfate group receiving 18mg/kg/d of elemental zinc orally topiramate group receiving topiramate 5mg/kg/d, orally and Topiaramate plus Zinc sulfate group receiving both zinc sulfate (18mg/kg/d) and topiramate (5mg/kg/d) orally for two weeks.Results: There were no significant differences with regard to all the three parameters in two-way ANOVA. The objectives of the present study were planned to analyze the alcohol de-addiction potential of oral zinc sulfate as a monotherapy and as a supplement to topiramate, in male wistar albino rats.Methods: Male wistar albino rats were exposed to ‘two-bottle free choice’ model of voluntary ethanol consumption, wherein each animal had access to water and 10% v/v ethyl alcohol in two separate bottles. Few indirect evidences support possible de-addiction potential of zinc being mediated through their interaction with nicotinic and NMDA receptors. Together our findings indicate that zinc is critical in determining the effects of ethanol at GlyRs and suggest that zinc binding at the D80 position may be important for mediating some of the behavioral effects of ethanol action at GlyRs.īackground: With regard to tobacco and alcohol addiction, involvement of NMDA receptors and glutamate as neurotransmitter has been highlighted. Other behavioral tests including ethanol induced motor incoordination and strychnine induced convulsions revealed no differences between the KI and WT mice. These KI mice showed decreased ethanol consumption and preference and displayed increased startle responses as compared to their WT littermates. Next, we evaluated the in vivo effects of the D80A substitution by using heterozygous Glra1(D80A) knock-in (KI) mice. Also, in contrast to what was seen with WT GlyRs, neither adding nor chelating zinc changed the magnitude of ethanol enhancement of mutant D80A receptors. At D80A GlyRs, the effects of 50 and 200 mM ethanol were reduced as compared to WT receptors. Here, we first investigated the effects of zinc on ethanol action at recombinant wild type (WT) and mutant α1 GlyRs containing the D80A substitution, which eliminates zinc potentiation. In addition, zinc ions also modulate GlyR function, and recent evidence suggests that physiological concentrations of zinc enhance ethanol potentiation of GlyRs. Among the protein targets of ethanol are glycine receptors (GlyRs), which are potentiated by millimolar concentrations of ethanol. Ethanol is a widely used drug, yet an understanding of its sites and mechanisms of action remains incomplete.
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