长期抗发作药物对人类血液中氧化素参数的影响
Danijel Jakovljević1,2, Milan Nikolić1, Vesna Jovanović1
1Department of Biochemistry, Faculty of Chemistry, University of Belgrade, 11158 Belgrade, Serbia.
Pharmaceuticals (Basel, Switzerland)
|January 23, 2024
概括
抗发作药物改变了氧化还原平衡. 拉莫特里金和卡巴马泽平在患者中显著改变了抗氧化酶配置文件,影响了超氧化物转化酶,催化酶和亚酸盐水平.
科学领域:
- 生物化学 生化学
- 神经科学是一个神经科学.
- 药理学 药理学是指药理学的学科.
背景情况:
- 影响全球数以百万计的人,但抗发作药物的对氧化还原平衡的影响仍然不太清楚.
- 氧化还原稳定在细胞功能和疾病发病过程中起着至关重要的作用.
研究的目的:
- 为了比较单独治疗拉莫特里金,卡巴马西平和氨酸对患者的氧化还原平衡的长期影响.
- 研究红细胞和血中抗氧化酶和氧化应激标记物的变化.
主要方法:
- 对抗氧化酶 (超氧化脱酶,酸酶,谷氨过氧化酶,谷氨减少酶) 和相关标记物 (血红蛋白,甲血红蛋白,总蛋白质,硫醇,酸盐,脂类过氧化物,总谷氨) 的分析.
- 在单一治疗 (lamotrigine,carbamazepine,valproate) 的患者和未经药物治疗的对照人群之间的比较.
- 使用正规差异分析来区分酶配置文件.
主要成果:
- 拉莫特里金治疗降低了超氧化物脱酶活性和醇和脂质过氧化物总度.
- 卡巴马泽平治疗增加了亚酸盐水平,并降低了超氧化物失调酶活性.
- 瓦尔酸盐治疗导致酶活性降低. 红细胞抗氧化酶的组成在拉莫特里金/卡巴马西平组和对照组之间有显著差异.
结论:
- 用抗发作药物的单疗法明显改变了氧化还原稳态.
- 特定的抗发作药物诱导抗氧化酶配置和氧化还原平衡的独特变化.
相关概念视频
Arteries of the Lower Limbs
190
Epilepsy is a chronic neurological disease marked by recurrent, unpredictable seizures. These seizures are caused by abnormal electrical discharges in the brain, leading to behavior, sensation, or consciousness alterations. They can also cause transient impairment of awareness, interfering with daily activities.
Various factors can trigger epilepsy, including genetic factors, brain damage, metabolic causes, and unknown etiology. Diagnosis of epilepsy involves electroencephalography (EEG), which...
Various factors can trigger epilepsy, including genetic factors, brain damage, metabolic causes, and unknown etiology. Diagnosis of epilepsy involves electroencephalography (EEG), which...
190
Antiepileptic Drugs: Potassium Channel Activators
183
Ezocgabine or retigabine, an antiepileptic drug of remarkable efficacy, has revolutionized the management of seizures. It is a potassium channel activator, explicitly targeting the family of Q subtype potassium channels. It enhances the transmembrane potassium currents, regulating neuronal excitability. This action stabilizes the resting membrane potential, a pivotal factor in mitigating the hyperexcitability that characterizes epilepsy.
Ezogabine has gained approval as an adjunctive treatment...
Ezogabine has gained approval as an adjunctive treatment...
183
Antiepileptic Drugs: Modulators of Neurotransmitter Release Mediated by SV2A Protein
304
Antiepileptic drugs, such as levetiracetam (Keppra) and brivaracetam (Briviact), have emerged as crucial tools in managing epilepsy. These medications exert their therapeutic effects by targeting the synaptic vesicle protein SV2A, a transmembrane glycoprotein primarily found in the brain.
SV2A is a transmembrane glycoprotein located predominantly in the brain, modulating the release of neurotransmitters for neuronal communication. Both levetiracetam and brivaracetam exhibit a high affinity for...
SV2A is a transmembrane glycoprotein located predominantly in the brain, modulating the release of neurotransmitters for neuronal communication. Both levetiracetam and brivaracetam exhibit a high affinity for...
304
Antiepileptic Drugs: Sodium Channel Blockers
574
Antiepileptic drugs are specialized medications that prevent seizures in individuals diagnosed with epilepsy. These drugs primarily function by blocking the movement of sodium ions through channels in the neuronal membrane, inhibiting the repetitive firing of action potentials often associated with seizures.
Sodium channel blockers modulate ion channels, particularly voltage-gated sodium channels. They block only sodium ion movement.
Among the most commonly prescribed antiepileptic drugs are...
Sodium channel blockers modulate ion channels, particularly voltage-gated sodium channels. They block only sodium ion movement.
Among the most commonly prescribed antiepileptic drugs are...
574
Antiepileptic Drugs: Calcium Channel Blockers
405
Calcium channel blockers, a class of antiepileptic drugs, regulate the flow of calcium ions within neurons.
Calcium channel blockers exert their antiepileptic effects by targeting T-type calcium channels, which are integral to transmitting nerve signals in the central nervous system. These channels allow the passage of calcium ions, which are vital for neuronal communication. By inhibiting T-type calcium channels, calcium channel blockers effectively reduce the release of neurotransmitters and...
Calcium channel blockers exert their antiepileptic effects by targeting T-type calcium channels, which are integral to transmitting nerve signals in the central nervous system. These channels allow the passage of calcium ions, which are vital for neuronal communication. By inhibiting T-type calcium channels, calcium channel blockers effectively reduce the release of neurotransmitters and...
405


