s-allylcysteine and Psychomotor-Agitation

s-allylcysteine has been researched along with Psychomotor-Agitation* in 1 studies

Other Studies

1 other study(ies) available for s-allylcysteine and Psychomotor-Agitation

Article	Year
S-Allylcysteine prevents the rat from 3-nitropropionic acid-induced hyperactivity, early markers of oxidative stress and mitochondrial dysfunction. Neuroscience research, 2006, Volume: 56, Issue:1 We investigated the effects of S-allylcysteine (SAC) on early behavioral alterations, striatal changes in superoxide dismutase (SOD) activity, lipid peroxidation (LP) and mitochondrial dysfunction induced by the systemic infusion of 3-nitropropionic acid (3-NPA) to rats. SAC (300 mg/kg, i.p.), given to animals 30 min before 3-NPA (30 mg/kg, i.p.), prevented the hyperkinetic pattern evoked by the toxin. In addition, 3-NPA alone produced decreased activities of manganese- (Mn-SOD) and copper/zinc-dependent superoxide dismutase (Cu,Zn-SOD), increased LP (evaluated as the formation of lipid fluorescent products) and produced mitochondrial dysfunction in the striatum (measured as decreased 3-(3,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide reduction). In contrast, pretreatment of 3-NPA-injected rats with SAC resulted in a significant prevention of all these markers. Our findings suggest that the protective actions of SAC are related with its antioxidant properties, which in turn may be accounting for the preservation of SOD activity and primary mitochondrial tasks. Topics: Akathisia, Drug-Induced; Animals; Antineoplastic Agents; Behavior, Animal; Biomarkers; Convulsants; Corpus Striatum; Cysteine; Isoenzymes; Lipid Peroxidation; Male; Mitochondria; Nitro Compounds; Oxidative Stress; Propionates; Psychomotor Agitation; Rats; Rats, Wistar; Superoxide Dismutase	2006

Article

Year

S-Allylcysteine prevents the rat from 3-nitropropionic acid-induced hyperactivity, early markers of oxidative stress and mitochondrial dysfunction.

Neuroscience research, 2006, Volume: 56, Issue:1

We investigated the effects of S-allylcysteine (SAC) on early behavioral alterations, striatal changes in superoxide dismutase (SOD) activity, lipid peroxidation (LP) and mitochondrial dysfunction induced by the systemic infusion of 3-nitropropionic acid (3-NPA) to rats. SAC (300 mg/kg, i.p.), given to animals 30 min before 3-NPA (30 mg/kg, i.p.), prevented the hyperkinetic pattern evoked by the toxin. In addition, 3-NPA alone produced decreased activities of manganese- (Mn-SOD) and copper/zinc-dependent superoxide dismutase (Cu,Zn-SOD), increased LP (evaluated as the formation of lipid fluorescent products) and produced mitochondrial dysfunction in the striatum (measured as decreased 3-(3,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide reduction). In contrast, pretreatment of 3-NPA-injected rats with SAC resulted in a significant prevention of all these markers. Our findings suggest that the protective actions of SAC are related with its antioxidant properties, which in turn may be accounting for the preservation of SOD activity and primary mitochondrial tasks.

Topics: Akathisia, Drug-Induced; Animals; Antineoplastic Agents; Behavior, Animal; Biomarkers; Convulsants; Corpus Striatum; Cysteine; Isoenzymes; Lipid Peroxidation; Male; Mitochondria; Nitro Compounds; Oxidative Stress; Propionates; Psychomotor Agitation; Rats; Rats, Wistar; Superoxide Dismutase

2006