Oxidative stress in children affected by epileptic encephalopathies

Grosso, Salvatore; Longini, Mariangela; Rodriguez, Antonello; Proietti, Fabrizio; Piccini, Barbara; Balestri, Paolo; Buonocore, Giuseppe

doi:10.1016/j.jns.2010.09.017

Cited by 29 publications

(25 citation statements)

References 32 publications

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“…The precursors of γ-Ks, F 2 -IsoPs, have been detected in patients with a variety of pathological conditions including AD, Huntington’s disease, Creutzfeldt-Jakob disease, multiple sclerosis and recently in children with epilepsy (Greco et al, 1999; Grosso et al, 2011; Minghetti et al, 2000; Montine et al, 1999; Montine et al, 1998). IsoFurans, which are produced under conditions of increased oxygen tension, have been found in disease-affected brain regions from Parkinson’s disease patients (Fessel et al, 2003).…”

Section: Discussionmentioning

confidence: 99%

Scavenging of highly reactive gamma-ketoaldehydes attenuates cognitive dysfunction associated with epileptogenesis

Pearson

Warren

Liang

et al. 2017

Neurobiology of Disease

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Cognitive dysfunction is a major comorbidity of the epilepsies; however, treatments targeting seizure-associated cognitive dysfunction, particularly deficits in learning and memory are not available. Isoketals and Neuroketals, collectively known as gamma-ketoaldehydes are formed via the non-enzymatic, free radical catalyzed oxidation of arachidonic acid and docosahexaenoic acid, respectively. They are attractive candidates for oxidative protein damage and resultant cognitive dysfunction due to their formation within the plasma membrane and their high proclivity to form cytotoxic adducts on protein lysine residues. We tested the hypothesis that gamma-ketoaldehydes mechanistically contribute to seizure-associated memory impairment using a specific gamma-ketoaldehyde scavenger, salicylamine in the kainic acid and pilocarpine rat models of temporal lobe epilepsy. We show that gamma-ketoaldehydes are increased following epileptogenic injury in hippocampus and perirhinal cortex, two brain regions imperative for learning and memory. Treatment with an orally bioavailable, brain permeable scavenger, salicylamine attenuated 1) spatial memory deficits 2) reference memory deficits and 3) neuronal loss and astrogliosis in two mechanistically distinct models of epilepsy without affecting the epileptogenic injury or the development of chronic epilepsy. We have previously demonstrated that reactive oxygen species and the lipid peroxidation biomarkers, F2-isoprostanes are produced following status epilepticus. However, which reactive species specifically mediate oxidative damage to cellular macromolecules remains at large. We provide novel data suggesting that memory impairment occurs via gamma-ketoaldehyde production in two models of epilepsy and that treatment with a gamma-ketoaldehyde scavenger can protect vulnerable neurons. This work suggests a novel target and therapy to treat seizure-induced memory deficits in epilepsy.

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Section: Discussionmentioning

confidence: 99%

Scavenging of highly reactive gamma-ketoaldehydes attenuates cognitive dysfunction associated with epileptogenesis

Pearson

Warren

Liang

et al. 2017

Neurobiology of Disease

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“…The formation of ROS is subsequently increased, which may potentially entail adverse effects inducing any kind of free radical-related disease [34,35,36,37,38]. Studies in which samples of cord blood or venous blood of newborns were investigated have shown that children are born with a low antioxidative status [33].…”

Section: Discussionmentioning

confidence: 99%

“…Some perinatological diseases of mother and child are associated with excessive radical formation. Preeclampsia [34], premature rupture of the membranes [35], necrotising enterocolitis [36], retinopathy of prematurity [37] and periventricular leukomalacia [38] are only a few examples of free radical-related diseases.…”

Section: Introductionmentioning

confidence: 99%

Non-Invasive Spectroscopic Determination of the Antioxidative Status of Gravidae and Neonates

Lademann

Gerber²,

Olbertz³

et al. 2015

Skin Pharmacol Physiol

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Pregnancy and postpartum adaptation cause an increased formation of free radicals. This is associated with various perinatological diseases, e.g. necrotising enterocolitis. The human body has developed a protective system in the form of the antioxidative potential. The present study was the first to investigate the kinetics of the cutaneous antioxidative status in pregnant women and newborns using a non-invasive spectroscopic method. Eighteen pregnant women and their babies took part in the study. A light-emitting diode-based compact scanner system was used for quick non-invasive measurements of carotenoid antioxidants in human skin based on reflection spectroscopy. It could be shown that the antioxidative status of the expectant mothers significantly declined during labour (p < 0.001) and on day 1 after delivery (p < 0.01). Compared to the mothers, the newborns exhibited a significantly higher cutaneous carotenoid concentration on both day 1 (p < 0.01) and 5 (p < 0.01) after delivery. These results suggest that the oxidative stress due to postpartum adaptation is counteracted by an enhanced reservoir of carotenoid antioxidants in the subcutaneous fatty tissue. The peripartum cutaneous carotenoid level of mothers declines continuously, whereas term newborns show very high cutaneous antioxidant values.

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“…These include genetic factors, intracellular electrolyte metabolism disorders leading to increased glutamatergic cell toxicity, mitochondrial dysfunction, oxidative stress, reduced growth factor, and increased cytokine concentration. [1][2][3][4] Experimental and clinical studies have suggested that free radicals may be involved in the pathogenesis of epilepsy. Oxidative stress is known to occur following acute seizure activity but its contributions during epileptogenesis are largely unknown.…”

Section: Introductionmentioning

confidence: 99%

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

Tüfekçi¹,

Koyuncuoğlu²,

Kırbaş³

et al. 2013

Epilepsi

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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 ...

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Oxidative stress in children affected by epileptic encephalopathies

Cited by 29 publications

References 32 publications

Scavenging of highly reactive gamma-ketoaldehydes attenuates cognitive dysfunction associated with epileptogenesis

Scavenging of highly reactive gamma-ketoaldehydes attenuates cognitive dysfunction associated with epileptogenesis

Non-Invasive Spectroscopic Determination of the Antioxidative Status of Gravidae and Neonates

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

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