Effects of chronic haloperidol and/or clozapine on oxidative stress parameters in rat brain

被引:16
作者
Agostinho, Fabiano R.
Jornada, Luciano K.
Schroder, Nadja
Roesler, Rafael
Dal-Pizzol, Felipe
Quevedo, Joao [1 ]
机构
[1] Univ Extreme Sul Catarinese, Programa PosGrad Ciencias Saude, Lab Neurociencias, BR-88806000 Criciuma, SC, Brazil
[2] Pontifical Catholic Univ, Fac Biosci, Neurobiol & Dev Biol Lab, BR-90619900 Porto Alegre, RS, Brazil
[3] Univ Fed Rio Grande do Sul, Inst Basic Hlth Sci, Dept Pharmacol, BR-90046900 Porto Alegre, RS, Brazil
[4] Univ Extreme Sul Catarinese, Programa PosGrad Ciencias Saude, Lab Fisiopatol Expt, BR-88806000 Criciuma, SC, Brazil
关键词
haloperidol; clozapine; oxidative stress; reactive oxygen species; antioxidant enzymes; peroxidative damage; schizophrenia; tardive dyskinesia;
D O I
10.1007/s11064-007-9311-3
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 [生物化学与分子生物学]; 081704 [应用化学];
摘要
Decreased antioxidant activity is considered as one of the causes of tardive dyskinesia in schizophrenic patients in a prolonged neuroleptic treatment course. Haloperidol (HAL) has been hypothesized to increase oxidative stress, while clozapine (CLO) would produce less oxidative damage. The objective was to determine whether CLO for 28 days could reverse or attenuate HAL-induced oxidative damage in animals previously treated with HAL for 28 days. HAL significantly increased thiobarbituric acid reactive substances levels in the cortex (CX) and striatum and increased protein carbonyls in hippocampus (HP) and CX and this was not attenuated by CLO treatment. In the total radical trapping antioxidant parameter assay there was a decrease in the HP total antioxidant potential induced by HAL and by treatment with HAL + CLO. Our findings demonstrated that the atypical antipsychotic CLO could not revert oxidative damage caused by HAL.
引用
收藏
页码:1343 / 1350
页数:8
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