Modulation of Antioxidant Enzymatic Activities by Certain Antiepileptic Drugs (Valproic Acid, Oxcarbazepine, and Topiramate): Evidence in Humans and Experimental Models

Cárdenas-Rodríguez, Noemi; Coballase-Urrutía, Elvia; Rivera-Espinosa, Liliana; Romero-Toledo, Arantxa; Sampieri, Alicia; Ortega-Cuéllar, Daniel; Montesinos-Correa, Hortencia; Floriano-Sánchez, Esaú; Carmona-Aparicio, Liliana

doi:10.1155/2013/598493

Cited by 40 publications

(27 citation statements)

References 70 publications

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“…(For migraine preventive medications, the case is less clear: Flunarizine, propranolol, and topiramate appear to be antioxidants, either directly or by raising levels of antioxidant enzymes, while valproate and amitriptyline appear to be pro‐oxidants. )…”

Section: Discussionmentioning

confidence: 99%

Migraine Triggers and Oxidative Stress: A Narrative Review and Synthesis

2015

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Section: Discussionmentioning

confidence: 99%

Migraine Triggers and Oxidative Stress: A Narrative Review and Synthesis

2015

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“…Thus, increased MPO enzyme activity indirectly indicates a decrease in NO level. Also, TPM increases NO release by inducing the NO synthase enzyme (30). Because of decreased NO levels, the production of asymmetric dimethyl arginine is increased, and this causes endothelial dysfunction.…”

Section: Discussionmentioning

confidence: 99%

Topiramate Reduces Aortic Cross-Clamping-Induced Lung Injury in Male Rats

Kurt

Kalkan

Türüt

et al. 2018

Acta Med. (Hradec Kralove, Czech Repub.)

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A B ST R AC T Background: Topiramate (TPM) decreases cytokine release and generation of reactive oxygen species (ROS). Cytokine and endothelin-1 (ET-1) secretion and ROS formation play an important role in ischemia-reperfusion (I/R) injury. We aimed to evaluate whether TPM prevents damage occurring in lung tissue during I/R. Materials and Methods: A total of 27 Wistar albino rats were divided into three groups of nine. To the I/R group, two hours of ischemia via infrarenal abdominal aorta cross-ligation and then two hours of reperfusion process were applied. TPM (100 mg/kg/day) orally for seven days was administered in the TPM treatment group. After the last dose of TPM treatment, respectively, two hours of ischemia and two hours of reperfusion were applied in this group. Results: Tumor necrosis factor-alpha (TNF-α) (p < 0.05), malondialdehyde (MDA) (p < 0.05), myeloperoxidase (MPO) (p < 0.05) and ET-1 (p < 0.05) levels of TPM treatment group's lung tissue were significantly lower than for the I/R group. Caspase-3 and histopathological damage were rather lower than that of the I/R group. Conclusions: During I/R, lung damage occurs due to excessive TNF-α and ET-1 release and ROS generation. TPM could well reduce development of lung damage by decreasing cytokine and ET-1 release and levels of ROS produced. K E Y WO R D S Topiramate; ischemia-reperfusion; lung injury; tumor necrosis factor-alpha; endothelin-1

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“…VPA is also histone deacetylase (HDAC) inhibitor and has a neuroprotective role [ 196 ]. A review by Cárdenas-Rodríguez et al summarizes the effects of AEDs on the markers of oxidative stress in human epileptic patients [ 197 ]. Although AEDs control seizures, their role to elicit systemic toxicity and to contribute to oxidative stress needs to be carefully considered during therapy.…”

Section: Treatment Options For Tlementioning

confidence: 99%

Seizure-Induced Oxidative Stress in Temporal Lobe Epilepsy

Puttachary

Sharma

Stark

et al. 2015

BioMed Research International

193

149

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An insult to the brain (such as the first seizure) causes excitotoxicity, neuroinflammation, and production of reactive oxygen/nitrogen species (ROS/RNS). ROS and RNS produced during status epilepticus (SE) overwhelm the mitochondrial natural antioxidant defense mechanism. This leads to mitochondrial dysfunction and damage to the mitochondrial DNA. This in turn affects synthesis of various enzyme complexes that are involved in electron transport chain. Resultant effects that occur during epileptogenesis include lipid peroxidation, reactive gliosis, hippocampal neurodegeneration, reorganization of neural networks, and hypersynchronicity. These factors predispose the brain to spontaneous recurrent seizures (SRS), which ultimately establish into temporal lobe epilepsy (TLE). This review discusses some of these issues. Though antiepileptic drugs (AEDs) are beneficial to control/suppress seizures, their long term usage has been shown to increase ROS/RNS in animal models and human patients. In established TLE, ROS/RNS are shown to be harmful as they can increase the susceptibility to SRS. Further, in this paper, we review briefly the data from animal models and human TLE patients on the adverse effects of antiepileptic medications and the plausible ameliorating effects of antioxidants as an adjunct therapy.

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Modulation of Antioxidant Enzymatic Activities by Certain Antiepileptic Drugs (Valproic Acid, Oxcarbazepine, and Topiramate): Evidence in Humans and Experimental Models

Cited by 40 publications

References 70 publications

Migraine Triggers and Oxidative Stress: A Narrative Review and Synthesis

Migraine Triggers and Oxidative Stress: A Narrative Review and Synthesis

Topiramate Reduces Aortic Cross-Clamping-Induced Lung Injury in Male Rats

Seizure-Induced Oxidative Stress in Temporal Lobe Epilepsy

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