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首页> 外文期刊>Pharmacology, Biochemistry and Behavior >Coenzyme Q10 does not prevent oral dyskinesias induced by long-term haloperidol treatment of rats.
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Coenzyme Q10 does not prevent oral dyskinesias induced by long-term haloperidol treatment of rats.

机译：辅酶Q10不能预防氟哌啶醇的长期治疗引起的大鼠口腔运动障碍。

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摘要

Tardive dyskinesia (TD) is a debilitating side effect of long-term treatment with neuroleptics with an unclear pathophysiologic basis. It has been proposed that TD may be a result of neuroleptic-induced oxidative stress. To investigate this hypothesis, we studied if neuroleptic-induced oral dyskinesias in rats, a putative analogue to human TD, could be prevented by the antioxidant coenzyme Q10 (CoQ10). Rats received 16 weeks of treatment with haloperidol decanoate (HAL) IM alone or together with orally administered CoQ10, and the behavior was recorded during and after treatment. HAL significantly increased the level of oral dyskinesias, and the increase persisted for 12 weeks after drug withdrawal. Cotreatment with CoQ10 did not attenuate the development of HAL-induced oral dyskinesia. Despite adequate absorption of orally administered CoQ10, shown by the increased serum levels of CoQ10, no increase of either CoQ10 or coenzyme Q9 was detected in the brain. These results suggest that cotreatment with CoQ10 does not inhibit the development of HAL-induced oral dyskinesias in rats, and that further studies seem to be needed in order to clarify the pharmacokinetics of CoQ10 in rats.
机译：迟发性运动障碍（TD）是长期服用抗精神病药物治疗，其病理生理基础尚不清楚的副作用。已经提出TD可能是精神安定药诱导的氧化应激的结果。为了研究该假设，我们研究了抗氧化剂辅酶Q10（CoQ10）是否可以预防神经衰弱诱导的大鼠口腔运动障碍（一种假定的人类TD类似物）。大鼠单独或与口服CoQ10一起接受癸酸氟哌啶醇（HAL）IM治疗16周，并在治疗期间和之后记录其行为。 HAL显着增加了口服运动障碍的水平，并且这种停滞现象在停药后持续了12周。与辅酶Q10共同治疗并不能减弱HAL引起的口腔运动障碍的发展。尽管口服CoQ10的吸收充分，如血清CoQ10水平升高所显示，但在大脑中未检测到CoQ10或辅酶Q9的增加。这些结果表明，辅酶Q10的共处理不会抑制大鼠HAL引起的口腔运动障碍的发展，而且为了阐明辅酶Q10在大鼠中的药代动力学，似乎还需要进一步的研究。

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