Agostinho Fabiano R, Jornada Luciano K, Schröder Nadja, Roesler Rafael, Dal-Pizzol Felipe, Quevedo João
Laboratório de Neurociências, Programa de Pós-Graduação em Ciências da Saúde, Universidade do Extremo Sul Catarinense, Criciuma, Santa Catarina, Brazil.
Neurochem Res. 2007 Aug;32(8):1343-50. doi: 10.1007/s11064-007-9311-3. Epub 2007 Mar 31.
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.
抗氧化活性降低被认为是精神分裂症患者在长期使用抗精神病药物治疗过程中发生迟发性运动障碍的原因之一。有假说认为,氟哌啶醇(HAL)会增加氧化应激,而氯氮平(CLO)产生的氧化损伤较少。目的是确定连续28天给予CLO是否能逆转或减轻先前连续28天给予HAL所致的动物氧化损伤。HAL显著增加了皮质(CX)和纹状体中的硫代巴比妥酸反应性物质水平,并增加了海马(HP)和CX中的蛋白质羰基化水平,而CLO治疗并未使其减弱。在总自由基捕获抗氧化参数测定中,HAL及HAL + CLO治疗均导致HP的总抗氧化能力下降。我们的研究结果表明,非典型抗精神病药物CLO不能逆转HAL所致的氧化损伤。