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首页> 外文期刊>Neurochemistry International: The International Journal for the Rapid Publication of Critical Reviews, Preliminary and Original Research Communications in Neurochemistry >Cocaine-induced status epilepticus and death generate oxidative stress in prefrontal cortex and striatum of mice.
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Cocaine-induced status epilepticus and death generate oxidative stress in prefrontal cortex and striatum of mice.

机译：可卡因引起的癫痫持续状态和死亡在小鼠的前额叶皮层和纹状体中产生氧化应激。

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Oxidative stress (OS) has been related to cocaine's actions and also to numerous nervous system pathologies, including seizures. The purpose of this work was to determine the alterations in glutathione (GSH) content, nitriteitrate and MDA levels after cocaine-induced toxicity. Male Swiss mice were injected (i.p.) with cocaine 90 mg/kg and observed during 1h. After this cocaine overdose some animals presented status epilepticus (SE) while some died after seizures. These animals were divided in two groups, SE and death. A group with an association of the antioxidant Vitamin E (Vit E, 400mg/kg, i.p.) plus Coc 90 (Vit E plus Coc 90) was undertaken to assess the neuroprotective effect of Vit E. Neurochemical analyses were carried out in prefrontal cortex (PFC) and striatum (ST). GSH levels increased only after cocaine-induced death in both areas studied. Cocaine-induced SE has increased nitriteitrate content in PFC and ST, while after death the increase was only in PFC. MDA (the lipid peroxidation marker) was elevated after SE and death in ST and only after death in PFC. Antioxidant treatment significantly reduced the GSH, nitriteitrate in ST and MDA levels. Only nitriteitrate content in PFC has not been decreased by Vit E pretreatment. The results relate that oxidative stress occurs after cocaine-induced toxicity mainly after death indicating that probably the increase of OS in the animal's brain leads to seizures and death, also showing a protective effect of Vit E in this process. Together with previous results this study contributes to the knowledge of cocaine-induced toxicity and possible in the near future to the use of antioxidants in the prevention of cocaine-induced CNS toxicity.
机译：氧化应激（OS）与可卡因的作用以及许多神经系统疾病（包括癫痫发作）有关。这项工作的目的是确定可卡因诱导的毒性后谷胱甘肽（GSH）含量，亚硝酸盐/硝酸盐和MDA含量的变化。向雄性瑞士小鼠注射（i.p.）可卡因90 mg / kg，并在1小时内观察到。可卡因用药过量后，一些动物表现出癫痫状态（SE），而另一些动物则在癫痫发作后死亡。将这些动物分为SE和死亡两组。一组由抗氧化剂维生素E（Vit E，400mg / kg，ip）加Coc 90（Vit E加Coc 90）组成的组来评估Vit E的神经保护作用。在前额叶皮层（ PFC）和纹状体（ST）。在两个研究区域中，仅在可卡因诱发的死亡后，GSH水平才增加。可卡因诱导的SE增加了PFC和ST中亚硝酸盐/硝酸盐的含量，而死亡后仅在PFC中增加。 SE和SE中死亡后，仅在PFC中死亡后，MDA（脂质过氧化标记）升高。抗氧化剂处理可显着降低ST和MDA中的GSH，亚硝酸盐/硝酸盐含量。 Vit E预处理仅降低了PFC中的亚硝酸盐/硝酸盐含量。结果表明，可卡因引起的毒性反应主要发生在死亡后发生氧化应激反应，这表明动物脑中OS的升高可能导致癫痫发作和死亡，在此过程中也显示出Vit E的保护作用。连同先前的结果，这项研究有助于了解可卡因诱发的毒性，并可能在不久的将来使用抗氧化剂预防可卡因诱发的中枢神经系统毒性。

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