No evidence for oxidative damage in the hippocampus after acute and chronic electroshock in rats

Barichello, Tatiana; Bonatto, Fernanda; Martins, Márcio Rodrigo; Moreira, José Cláudio Fonseca; Dal‐Pizzol, Felipe; Izquierdo, Iván; Quevedo, Joao L De

doi:10.1016/j.brainres.2004.04.026

Cited by 30 publications

(41 citation statements)

References 27 publications

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“…This hypothesis was not tested in this work. Previous work from our group has shown that an electroconvulsive shock was able to provoke an adaptive response of the hippocampus antioxidant enzymatic system [Barichello et al, 2004]. Barichello et al [2004] obtained an inverse ''U'' time curve in parameters of lipid and protein oxidative damage during a time period of 30 days after electroconvulsive shock.…”

Section: Discussionmentioning

confidence: 95%

“…Previous work from our group has shown that an electroconvulsive shock was able to provoke an adaptive response of the hippocampus antioxidant enzymatic system [Barichello et al, 2004]. Barichello et al [2004] obtained an inverse ''U'' time curve in parameters of lipid and protein oxidative damage during a time period of 30 days after electroconvulsive shock. We think that a chronic (30 days or more; 7½ h/day) irradiation could induce free radicals increase without cellular adaptation and consequent increase in biomolecule oxidative damage.…”

Section: Discussionmentioning

confidence: 95%

“…Results already published by our laboratory have shown that oxidant agents could increase the generation of carbonyl groups (protein oxidative damage) [Klamt et al, 2002;Barichello et al, 2004;Polydoro et al, 2004;Bonatto et al, 2005] and malondialdehyde (MDA) products (lipid oxidative damage) [Klamt et al, 2002;Barichello et al, 2004;Polydoro et al, 2004;Bonatto et al, 2005;Lima et al, 2005] and also lead to changes in the non-enzymatic antioxidant status [Polydoro et al, 2004] in different brain structures. All these previously published results were achieved using the same assays used in the present work.…”

Section: Assaysmentioning

confidence: 97%

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Oxidative stress effects on the central nervous system of rats after acute exposure to ultra high frequency electromagnetic fields

Ferreira

Bonatto

Pasquali

et al. 2006

Bioelectromagnetics

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Mobile telephones and their base stations are an important source of ultra high frequency electromagnetic fields (UHF-EMFs; 800-1800 MHz) and their utilization is increasing all over the world. Epidemiological studies have suggested that low energy UHF-EMFs may have biological effects, such as changes in oxidative metabolism after exposure. Therefore, we have investigated the effect of acute UHF-EMF exposure on non-enzymatic antioxidant defense and lipid and protein oxidative damage in the rat frontal cortex and hippocampus. We have used malondialdehyde (MDA) and carbonyl assays to assess lipid and protein oxidative damages, respectively. No changes in lipid and protein damage, and also in non-enzymatic defense were found in frontal cortex or hippocampus. These results suggest that acute UHF-EMF exposure is not able to produce detectable oxidative stress in rats from any age tested. However, more tests using a longer period of exposure and evaluating other tissues are necessary to ensure that there is no health risk associated with the use of mobile phones.

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Section: Discussionmentioning

confidence: 95%

Section: Discussionmentioning

confidence: 95%

Section: Assaysmentioning

confidence: 97%

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Oxidative stress effects on the central nervous system of rats after acute exposure to ultra high frequency electromagnetic fields

Ferreira

Bonatto

Pasquali

et al. 2006

Bioelectromagnetics

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“…Similar to our results Erakovic et al (10) reported that single or repeated ECS induced a decrease in SOD and glutation peroxidase (GPX) activities at various brain regions in rats. Baricello et al (11) demonstrated an increase in catalase (CAT) and SOD activities, a decrease in lipid peroxidation, and protein damage in the hippocampus immediately after and up to 30 days after a single or multiple ECS. Feier et al (4) found a delayed increase in oxidative damage after ECS and a decrease in SOD and CAT activities in hippocampus and striatum in rats.…”

Section: Discussionmentioning

confidence: 99%

“…While some researchers found an increase (4) in oxidants, others measured a decrease (11); meanwhile, Jornada et al [12] reported no significant changes in oxidative metabolites after ECS. Regarding antioxidants, Erakovic et al (10) and Feier et al [4] measured a decrease, but Baricello et al (11) found an increase.…”

Section: Introductionmentioning

confidence: 97%

Depresyonda EKT Sonrası Süperoksit Dismutaz Aktivitesi Düşüyor ve EKT'ye Kötü Yanıtla Korelasyon Gösteriyor

Virit¹,

Dalkılıç²,

Bulut³

et al. 2011

Npa

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ÖZET Amaç:Elektrokonvülzif tedavinin (EKT) oksidatif metabolizma üzerine etkileri ile ilgili literatürün ço¤u hayvan deneylerine dayanmaktad›r ve oksidan/antioksidan dengenin de¤iflti¤ine dair çeliflkili sonuçlar içermektedir. Bu alanda yap›lan ilk insan çal›flmas› olan bu çal›flman›n amac› depresif hastalarda EKT sonras› oksidan ve antioksidanlardaki de¤iflimleri araflt›rmakt›r. Yöntemler: On dört unipolar ve iki bipolar depresyon hastas› çal›flmaya dahil edildi. Kan örnekleri ilk EKT seans›ndan 1 saat once ve 7. EKT seans›ndan 1 saat sonra al›nd›. Plazmada oksidanlardan malondialdehit (MDA), nitrik oksit (NO) ve ksantin oksidaz (XO); antioksidanlardan süperoksit dismutaz (SOD) seviyeleri ölçüldü. Bulgular: Birinci ve 7. EKT seans›ndan sonraki Hamilton Depresyon Ölçe¤i (HAM-D) skorlar› 32.63±9.54 ve 16.50±7.22 idi (t=7.92, df=15, p<0.001). Yedinci EKT sonras› SOD de¤erleri EKT öncesi SOD de¤erlerinden anlaml› olarak düflüktü (p<0.05, Z= -3,459). EKT öncesi ve sonras› MDA, NO ve XO de¤erleri aras›nda anlaml› bir farkl›l›k yoktu (p>0.05). Bununla birlikte, EKT öncesi SOD de¤erleri EKT öncesi HAM-D skorlar› ile anlaml› düzeyde pozitif korelasyon gös-teriyordu (r=0.641, p=0.007). Sonuç: EKT sonras› antioksidan bir enzim olan SOD düzeyindeki düflüfl oksidatif stresi artt›rarak nöronlara zarar verebilir. Bu nedenle EKT uygulama dönemlerinde antioksidan ekleme tedavilerinin olas› faydalar› araflt›r›lmal›d›r. Yine EKT öncesi yüksek oksidan seviyeleri depresyon hastalar›nda EKT'ye kötü yan›t› yordayabilir. (Nöropsikiyatri Arflivi 2010; 47: 247-51) Anahtar kelimeler: Elektrokonvülzif tedavi, Oksidatif metabolizma, Süperoksit dismutaz ABSTRACT Objective: The literature regarding effects of electroconvulsive therapy (ECT) on oxidative metabolism (OM) reports conflicting changes in oxidant and antioxidant status in animal studies. The goal of this first human study was to investigate the changes in oxidants and antioxidants in plasma of depressed patients after ECT. Methods: Fourteen unipolar and two bipolar patients were included in the study. The blood samples were obtained within one hour before the 1 st and within one hour after the 7 th ECT sessions. Oxidants malondialdehyde (MDA), nitric oxide (NO), and xanthine oxidase (XO) and antioxidant superoxide dismutase (SOD) were measured in the plasma. Results: Before the 1 st and after the 7 th ECT sessions, the Hamilton Depression Rating Scale (HDRS) scores were 32.63±9. 54 and 16.50±7.22, respectively (t=7.92, df=15, p<0.001). After the 7 th ECT, SOD values were significantly lower than pre-ECT SOD values (p<0.05, Z= -3,459). There were no significant difference between pre-and post-ECT values of MDA, NO, and XO (p>0.05). However, pre-ECT SOD values were significantly and positively correlated with pre-ECT HDRS scores (r=0.641, p=0.007). Conclusion:The decrease in antioxidant enzyme SOD after ECT may damage the neurons by increasing oxidative stress. Thus, possible benefits of antioxidant supplementation during ECT should be investigated. Additionally, higher pre-ECT o...

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Acute Neuronal Injury

Fujikawa¹

2010

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), except for brief excerpts in connection with reviews or scholarly analysis. Use in connection with any form of information storage and retrieval, electronic adaptation, computer software, or by similar or dissimilar methodology now known or hereafter developed is forbidden. The use in this publication of trade names, trademarks, service marks, and similar terms, even if they are not identified as such, is not to be taken as an expression of opinion as to whether or not they are subject to proprietary rights.Cover illustration: The cover shows neurons in the piriform cortex of a control rat and a rat 24 hours after generalized seizures, showing seizure-induced translocation of endonuclease G (endoG) from cytoplasmic mitochondria to nuclei. The mitochondrial endoG is red and nuclei are blue in the control brain. Following seizures, nuclei appear purplish-white because of movement of endoG to nuclei.

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No evidence for oxidative damage in the hippocampus after acute and chronic electroshock in rats

Cited by 30 publications

References 27 publications

Oxidative stress effects on the central nervous system of rats after acute exposure to ultra high frequency electromagnetic fields

Oxidative stress effects on the central nervous system of rats after acute exposure to ultra high frequency electromagnetic fields

Depresyonda EKT Sonrası Süperoksit Dismutaz Aktivitesi Düşüyor ve EKT'ye Kötü Yanıtla Korelasyon Gösteriyor

Acute Neuronal Injury

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