苯妥英钠诱导cd-1小鼠外周血多染红细胞微核

Norberto Alarcón-Herrera, Saúl Flores-Maya
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引用次数: 0

摘要

癫痫发作是最常见的神经系统疾病之一,可为散发性或复发性(癫痫)危象。就癫痫患者而言,这些药物必须终生治疗,成为苯妥英处方中控制癫痫发作的主要药物。然而,尽管在市场上已经存在了几十年,关于它们的基因毒性作用的信息却很少。因此,本研究采用微核试验对小鼠小家鼠CD-1株进行了30天苯妥英基因毒性损伤的评价。结果表明,3种剂量的苯妥英(2.8、4.2和6.64 mg/kg)对小鼠染色体具有致裂性,且剂量越高,对小鼠染色体的损伤越大。此外,4.2和6.64 mg/kg剂量抑制细胞毒性损伤诱导细胞动力学。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
PHENYTOIN SODIUM INDUCED MICRONUCLEI IN THE POLYCHROMATIC ERYTHROCYTES OF CD-1 MOUSE PERIPHERAL BLOOD
Seizures are one of the most common neural disorders, and may be sporadic or recurrent (epilepsy) crisis. In the case of people with epilepsy, these must be treated throughout their lives, being a major phenytoin prescription for seizure control medicines out. However, despite having several decades in the market there is very little information about their genotoxic effects. Therefore in this study to evaluate the ability of phenytoin to induce genotoxic damage for 30 days using the micronucleus test in mice Mus musculus CD-1 strain. It was determined that the three doses of phenytoin used (2.8, 4.2 and 6.64 mg/kg) induced clastogenicity in mouse chromosomes, that at higher doses the damage is greater. Furthermore, also inhibiting cytotoxic damage induced cell kinetics for doses of 4.2 and 6.64 mg/kg.
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