ArticlePsychopharmacology2012
α-Lipoic acid, a scavenging agent for H₂O₂, reduces ethanol-stimulated locomotion in mice.
Article in Psychopharmacology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 20 citations in OpenAlex.
- Alpha-Lipoic Acid in Early-Stage Alcohol-Related Brain Damage in Rats: A Comparative Pilot Study.Molecules (Basel, Switzerland) · 2025Article
- Alpha-Lipoic Acid Reduces Methemoglobin and Oxidative Imbalance in the Blood and Liver Induced by Dapsone in Mice: Molecular Mechanism of Antioxidant Action.ACS pharmacology & translational science · 2025Article
- Pharmacological Antagonism of T-Type Calcium Channels Constrains Rebound Burst Firing in Two Distinct Subpopulations of GABA Neurons in the Rat Ventral Tegmental Area: Implications for α-Lipoic Acid.Frontiers in pharmacology · 2019Article
- Acquisition and reconditioning of ethanol-induced conditioned place preference in mice is blocked by the H₂O₂ scavenger alpha lipoic acid.Psychopharmacology · 2013Article
- Behavioral and biochemical evidence of the role of acetaldehyde in the motivational effects of ethanol.Frontiers in behavioral neuroscience · 2013Article
- Ethanol-derived acetaldehyde: pleasure and pain of alcohol mechanism of action.Frontiers in behavioral neuroscience · 2013Article
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
rationaleThe main system of central ethanol oxidation is mediated by the enzyme catalase. By reacting with H(2)O(2), brain catalase forms compound I (the catalase-H(2)O(2) system), which is able to oxidize ethanol to acetaldehyde in the brain. Previous studies have demonstrated that pharmacological manipulations of brain catalase activity modulate the stimulant effects of ethanol in mice. However, the role of H(2)O(2) in the behavioral effects of ethanol has not yet been clearly addressed.
objectivesIn the present study, we investigated the effects of alpha-lipoic acid (LA), a scavenging agent for H(2)O(2), on ethanol-induced locomotor stimulation.
methodsCD-1 mice were pretreated with LA [0-100 mg/kg, intraperitoneally (IP)] 0-60 min prior to administration of ethanol (0-3.75 g/kg, IP). In another experiment, animals were pretreated with LA (0, 25, or 50 mg/kg, IP) 30 min before cocaine (10 mg/kg, IP), amphetamine (2 mg/kg, IP), or caffeine (25 mg/kg, IP). After these treatments the animals were placed in an open-field chamber and their locomotor activity was measured for 20 min.
resultsLA 25, 50, and 100 mg/kg IP prevented ethanol-induced locomotor stimulation. LA did not affect the locomotor-stimulating effects of cocaine, amphetamine, and caffeine. Additionally, we demonstrated that LA prevents the inactivation of brain catalase by 3-amino-1,2,4-triazole, thus indicating that H(2)O(2) levels are reduced by LA.
conclusionsThese data support the idea that a decrease in cerebral H(2)O(2) production by LA administration inhibits ethanol-stimulated locomotion. This study suggests that the brain catalase-H(2)O(2) system, and by implication centrally formed acetaldehyde, plays a key role in the psychopharmacological effects of ethanol.
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