Main Article Content
Influence of N-Acetyl cysteine on selected extrapyramidal movement disorders and oxidative stress induced by haloperidol in rats
Abstract
Haloperidol (HAL) is a widely used neuroleptic drug for the treatment of acute and chronic psychosis. Its use is limited by its tendency to produce a range of extrapyramidal movement disorders such as, tardive dyskinesia (TD), akathisia, dystonia and parkinsonism. Increased levels of thiobarbituric-acid reactive products have been found in
the cerebrospinal fluid and plasma of patients treated with neuroleptics, especially those with movement disorders. HAL, is metabolized by an oxidase, generates large quantities of oxyradicals and a potent toxic pyridinium-like metabolite and induces oxidative stress. It is proposed to study the effect of n-acetyl cysteine (NAC) on selected extrapyramidal movement disorders (tardive dykinesia and catalepsy), total antioxidant status and lipid peroxidation induced by HAL. HAL (1 mg/kg/i.p) was injected for 21 days in rats, and NAC at doses of 30, 100 and 300 mg/kg dissolved in normal saline was administered,
intra-peritoneally once (30 minutes prior to haloperidol) on the last day of HAL treatment. NAC supplementation significantly decreased haloperidol induced TD and catalepsy dose dependently. However, further work is required to investigate the effect of chronic
administration of NAC in the improvement of TD so as to confirm the usefulness of NAC as
supplements for improved control of TD.
the cerebrospinal fluid and plasma of patients treated with neuroleptics, especially those with movement disorders. HAL, is metabolized by an oxidase, generates large quantities of oxyradicals and a potent toxic pyridinium-like metabolite and induces oxidative stress. It is proposed to study the effect of n-acetyl cysteine (NAC) on selected extrapyramidal movement disorders (tardive dykinesia and catalepsy), total antioxidant status and lipid peroxidation induced by HAL. HAL (1 mg/kg/i.p) was injected for 21 days in rats, and NAC at doses of 30, 100 and 300 mg/kg dissolved in normal saline was administered,
intra-peritoneally once (30 minutes prior to haloperidol) on the last day of HAL treatment. NAC supplementation significantly decreased haloperidol induced TD and catalepsy dose dependently. However, further work is required to investigate the effect of chronic
administration of NAC in the improvement of TD so as to confirm the usefulness of NAC as
supplements for improved control of TD.
