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SkQ-1 Regulates Xanthine Oxidase Activity in the Settings of Epilepsic Seizures in Rats

机译:SKQ-1调节黄嘌呤氧化酶活性在大鼠中的癫痫癫痫发作中

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摘要

Interdependence between mitochondrial dysfunctions and synthesis of the free radicals during the epileptogenesis is proved by number of publications. Xanthine Oxidase (XO) might serve as a source of hydrogen peroxide synthesis, which by its turn is able to disturb the process of ATP generation in mitochondria. Antioxidants, such as Skulachev's cations, might be used as possible inhibitors of XO and prevent the formation of free radicals in mitochondria. In our current work, we found out that SkQ-1 might inhibit the activity of XO in homogenate as well as in the purified fraction in vitro. In vivo modeling of epilepsy with the utility of korazol showed that the quantity of XO final product -uric acid, is elevating, whereas addition of SkQ-1 might suppress that increase in mitochondria.
机译:通过出版物的数量证明了对癫痫发生过程中的线粒体功能障碍和自由基的合成之间的相互依存。 黄嘌呤氧化酶(XO)可以作为过氧化氢合成的源,其转弯能够干扰线粒体中ATP生成的过程。 抗氧化剂如斯普拉赫夫的阳离子,可能用作XO的可能抑制剂,并防止在线粒体中形成自由基。 在我们目前的工作中,我们发现SKQ-1可能抑制XO在匀浆中的活性以及体外纯化的级分。 在癫痫的体内造型中,随着Korazol的效用表明,XO最终产品的数量 - 尿酸升高,而添加SKQ-1可能会抑制线粒体增加。

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