Selenium and Topiramate Modulates Brain Microsomal Oxidative Stress Values, Ca2+-ATPase Activity, and EEG Records in Pentylentetrazol-Induced Seizures in Rats

Nazıroğlu, Mustafa; Kutluhan, Süleyman; Yılmaz, Mustafa

doi:10.1007/s00232-008-9132-6

Cited by 82 publications

(63 citation statements)

References 46 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…ROS production in an uncontrolled fashion causes important damage to a wide range of biological molecules, such as DNA, lipids, proteins, carbohydrates, or any nearby molecule causing a cascade of chain reactions resulting in neuronal damage and epilepsy (Nazıroğlu, 2009). Oxidative stress has been implicated in the genesis and progression of epileptic seizures (Nazıroğlu et al, 2008;Kutluhan et al, 2009;Demirci et al, 2013). The ROS in the neurons of epileptic animals and humans are controlled by antioxidants, including melatonin (Table 2).…”

Section: Melatonin and Trp Channelsmentioning

confidence: 99%

Role of melatonin on calcium signaling and mitochondrial oxidativestress in epilepsy: focus on TRP channels

Nazıroğlu¹

2015

Turk J Biol

View full text Add to dashboard Cite

Calcium ion (Ca 2+ ) accumulation and excessive oxidative stress in the hippocampus and brain cortex have long been known as major contributors to the etiology of epilepsy. I have reviewed the role of Ca 2+ signaling through cation channels and mitochondriamediated oxidative stress on epilepsy in human and animals. A review of the relevant papers and results from recent studies were obtained from PubMed and the Science Citation Index. Current literature findings indicate that melatonin and agomelatine reduce activation of hippocampal transient receptor potential (TRP), glutamate receptors, and voltage-gated calcium channels that are critical for the development of abnormal Ca 2+ homeostasis and oxidative stress and associated mitochondrial dysfunction. In addition, low doses of melatonin induce anticonvulsant action through increase of GABA levels in the hippocampus and brain cortex. The accumulating evidence implicates a modulator role of melatonin on excessive oxidative stress products, plus mitochondrial and Ca 2+ dysregulations in epilepsy. The evidence indicates that modulation of oxidative stress and neuronal Ca 2+ handling occurs through effects on TRP channels, suggesting an increasingly viable approach for therapeutic interventions against epilepsy.

show abstract

Section: Melatonin and Trp Channelsmentioning

confidence: 99%

Role of melatonin on calcium signaling and mitochondrial oxidativestress in epilepsy: focus on TRP channels

Nazıroğlu¹

2015

Turk J Biol

View full text Add to dashboard Cite

show abstract

“…Furthermore, erythrocyte GR and plasma ascorbate and vitamin A concentrations were lower [79]. In the majority of these studies also increased markers of lipid peroxidation were noted [75,[77][78][79][80][81][82].…”

Section: Influence Of Aeds On Antioxidants and Markers Of Oxidative Smentioning

confidence: 91%

The Role of Reactive Species in Epileptogenesis and Influence of Antiepileptic Drug Therapy on Oxidative Stress

Martinc¹,

Grabnar²,

Vovk³

2012

Current Neuropharmacology

View full text Add to dashboard Cite

Abstract:Epilepsy is considered one of the most common neurological disorders. The focus of this review is the acquired form of epilepsy, with the development process consisting of three major phases, the acute injury phase, the latency epileptogenesis phase, and the phase of spontaneous recurrent seizures. Nowadays, an increasing attention is paid to the possible interrelationship between oxidative stress resulting in disturbance of physiological signalling roles of calcium and free radicals in neuronal cells and mitochondrial dysfunction, cell damage, and epilepsy. The positive stimulation of mitochondrial calcium signals by reactive oxygen species and increased reactive oxygen species generation resulting from increased mitochondrial calcium can lead to a positive feedback loop. We propose that calcium can pose both, physiological and pathological effects of mitochondrial function, which can lead in neuronal cell death and consequent epileptic seizures. Various antiepileptic drugs may impair the endogenous antioxidative ability to prevent oxidative stress. Therefore, some antiepileptic drugs, especially from the older generation, may trigger oxygen-dependent tissue injury. The prooxidative effects of these antiepileptic drugs might lead to enhancement of seizure activity, resulting in loss of their efficacy or apparent functional tolerance and undesired adverse effects. Additionally, various reactive metabolites of antiepileptic drugs are capable of covalent binding to macromolecules which may lead to deterioration of the epileptic seizures and systemic toxicity. Since neuronal loss seems to be one of the major neurobiological abnormalities in the epileptic brain, the ability of antioxidants to attenuate seizure generation and the accompanying changes in oxidative burden, further support an important role of antioxidants as having a putative antiepileptic potential.

show abstract

“…[31] A decrease in NO amounts is followed by a corresponding decrease in the GABA levels via an increase in the GABA transaminase activity. [32] Naziroglu et al [21] showed no differences in the NO levels in the brain cortex of rats when seizures were induced with PTZ. Ilhan et al [15,23] in two studies documented an increase in NO levels in the brain cortex of rats that had seizures induced with PTZ.…”

Section: Mda Determinationmentioning

confidence: 98%

“…This result is in accordance with the literature findings. [9,11,14,15,21,22] However, the results concerning antioxidant enzyme activities are somewhat conflicting. Discrepancies can be explained by methodological differences, or elevated enzyme activities may be reduced because of oxidative stress.…”

Section: Mda Determinationmentioning

confidence: 99%

“…Also, tiagabine and levetiracetam had no effect on the increase of NO levels; however, the rest of the AEDs were affected by an increase in the NO levels as dose-dependent. Naziroglu et al [21] showed that topiramate had no significant effect on MDA and NO levels in rat brain cortex. Bashkatova et al [11] reported that PTZ-induced MDA and NO levels have decreased with phenobarbitale, lamotrigine, phenazepam, meksidol, and α-tocopherol treatment.…”

Section: Mda Determinationmentioning

confidence: 99%

See 1 more Smart Citation

The Effects of Pregabalin on Cerebral Cortical Oxidative Stress of Rats on Pentylenetetrazole Induced Epileptic Seizure

Tüfekçi¹,

Koyuncuoğlu²,

Kırbaş³

et al. 2013

Epilepsi

View full text Add to dashboard Cite

SummaryObjectives: In this experimental model of epileptic seizure induced by pentylenetetrazole (PTZ), we aimed to investigate the effect of pregabalin, (PGB), (Lyrica(R)) in the brain cortex tissues and on superoxide dismutase (SOD) and catalase (CAT) activities as well as nitric oxide (NO) and malondialdehyde (MDA) levels, which are indicators of oxidative stress. Methods:Forty male Wistar rats were randomly divided into four equal groups. The first group was used as a control group. The second group received a single dose administration of PTZ. Third and fourth groups were given, via gastric gavage, doses of 100 mg/kg body weight/day of PGB, divided into two, for two days. Seizure is obtained by applying intraperitoneally (ip) 50 mg/kg body weight of PTZ to groups II and IV. After one hour of PTZ administration, all rats were sacrificed and brain cortex tissues were taken. SOD and CAT activities and NO and MDA levels were studied in the brain cortex tissues.Results: MDA levels and SOD activity of the PGB and PGB+PTZ groups were significantly lower than the control group ( p=0.005, p=0.001 and p=0.005, p=0.004, respectively), and NO level of the PGB and PGB+PTZ groups were significantly higher than the control group (p=0.001, p=0.001, respectively). CAT levels between the groups were similar. Conclusion:Our study results indicate that PGB prevents oxidative stress and increases NO levels in the rat brain cortical tissues during epileptic seizure. Increased NO may contribute to PGB's antiepileptic effect.Key words: Epilepsy; oxidative stress; pregabalin; pentylenetetrazole. ÖzetAmaç: Pentilentetrazol (PTZ) ile epileptik nöbet oluşturulan bu deneysel modelde, beyin korteksinde, oksidatif stresin göstergeleri olan sü-peroksit dismutaz (SOD), katalaz (CAT) aktiviteleri, nitrikoksit (NO) ve malondialdehit (MDA) düzeyleri üzerine pregabalinin (PGB) etkilerini araştırmayı amaçladık. Gereç ve Yöntem:Wistar cinsi 40 adet erkek sıçan rastgele 4 eşit gruba ayrıldı. İlk grup kontrol grubu olarak kullanıldı ve tek doz PTZ uygulanan grup, ikinci grup olarak kabul edildi. Üçüncü ve dördüncü gruba 100 mg/kg vücut ağırlığı/gün PGB ikiye bölünmüş dozlarda intragastrik yolla iki gün verildi. Grup II ve grup IV'e intraperitoneal (i.p.) (50 mg/kg vücut ağırlığı) PTZ uygulanarak nöbet oluşturuldu. PTZ uygulamasından bir saat sonra tüm sıçanlar sakrifiye edildi ve beyin korteksleri alındı. Beyin korteks dokularında SOD ve CAT aktiviteleri ile NO ve MDA düzeyleri çalışıldı.Bulgular: PGB ve PGB+PTZ gruplarında MDA düzeyi ve SOD aktivitesi, kontrol grubundan istatistiksel olarak daha düşük saptandı (sırasıyla p=0.005, p=0.001 ve p=0.005, p=0.004). PGB ve PGB+PTZ gruplarının NO düzeyi, kontrol grubundan istatistiksel olarak daha yüksekti (sırasıyla p=0.001, p=0.001). Gruplar arasındaki CAT düzeyleri benzerdi.Sonuç: Çalışmamızın sonuçları, PGB'nin oksidatif stresi önlediğini ve epileptik nöbet sırasında sıçan beyin korteks dokularında NO düzeylerini arttırdığını göstermiştir. Artmış olan NO düzeyinin PGB'in antiepileptik etkisine katkı ...

show abstract

Selenium and Topiramate Modulates Brain Microsomal Oxidative Stress Values, Ca2+-ATPase Activity, and EEG Records in Pentylentetrazol-Induced Seizures in Rats

Cited by 82 publications

References 46 publications

Role of melatonin on calcium signaling and mitochondrial oxidativestress in epilepsy: focus on TRP channels

Role of melatonin on calcium signaling and mitochondrial oxidativestress in epilepsy: focus on TRP channels

The Role of Reactive Species in Epileptogenesis and Influence of Antiepileptic Drug Therapy on Oxidative Stress

The Effects of Pregabalin on Cerebral Cortical Oxidative Stress of Rats on Pentylenetetrazole Induced Epileptic Seizure

Contact Info

Product

Resources

About