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      Neuropsychiatric Disease and Treatment (submit here)

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      Investigation of PON1 activity and MDA levels in patients with epilepsy not receiving antiepileptic treatment

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          Abstract

          Purpose

          There are many studies dedicated to researching the etiopathogenesis of epilepsy. In such research, oxidative and antioxidant indicators of etiopathogenesis have also been examined under the scope. Drawing on a group of patients with epilepsy who were receiving no treatment, we have tried to evaluate whether or not an increase in oxidative indicators is linked directly with the disorder, independent of epileptic medicaments.

          Methods

          Thirty people in good health and 30 newly diagnosed with epilepsy and who received ambulatory treatment in the polyclinic of the Neurology Department took part in the study. The tests relating to serum malondialdehyde (MDA) levels and paraoxonase 1 (PON1) activity were carried out in the biochemistry laboratory.

          Results

          Even though the levels of MDA in the patient group (14.34±3.59 nmol/mL) were found to be high compared to those of the control group, which consisted of people in good health (13.53±3.56 nmol/mL), there was no statistically significant difference. PON1 activity in the serum taken from people in the patient group (0.65±0.17) was lower in comparison to that observed in the serum of the control group (0.71±0.17 U/L). Nonetheless, it was not so low as to have significance from a statistical point of view.

          Conclusion

          We conclude that such a high level of oxidative parameters should have been related to the disease and that statistically significant findings that emerged in some other studies could have been related to an antiepileptic treatment.

          Most cited references21

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          Oxidative damage to RNA: mechanisms, consequences, and diseases.

          Overproduction of free radicals can damage cellular components resulting in progressive physiological dysfunction, which has been implicated in many human diseases. Oxidative damage to RNA received little attention until the past decade. Recent studies indicate that RNA, such as messenger RNA and ribosomal RNA, is very vulnerable to oxidative damage. RNA oxidation is not a consequence of dying cells but an early event involved in pathogenesis. Oxidative modification to RNA results in disturbance of the translational process and impairment of protein synthesis, which can cause cell deterioration or even cell death. In this review, we discuss the mechanisms of oxidative damage to RNA and the possible biological consequences of damaged RNA. Furthermore, we review recent evidence suggesting that oxidative damage to RNA may contribute to progression of many human diseases.
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            The epidemiology of epilepsy revisited.

            Epidemiology is the study of the dynamics of a medical condition in a population. There are many shortcomings in the understanding of the epidemiology of epilepsy mostly caused by methodological problems. These include diagnostic accuracy, case ascertainment, and selection bias. In this article recent progress in this area is discussed and suggestions for future research are made. It is generally accepted that in developed countries the incidence is around 50/100 000/year. In resource-poor countries, the incidence is likely to be higher. Prevalence of active epilepsy is in the range of 5-10/1000 in most locations, although it might be higher in some isolates. Age-specific incidence rates have changed, with a decrease in younger age groups and an increase in persons above 60 years. The overall prognosis for seizure control is good and over 70% will enter remission. Epilepsy carries an increased risk of premature death particularly in patients with chronic epilepsy. Sudden unexpected death has been increasingly recognized as a major culprit for this increased mortality. There is geographic variation in the incidence of epileptic syndromes likely to be associated with genetic and environmental factors, although as yet causality has not been fully established. The complete range of aetiologies in the general population is not known. Few predictors of outcome are recognized and it is difficult to prognosticate in any individual case. Knowledge is patchy about the epidemiology of sudden unexpected death in epilepsy. Future epidemiological research needs to address these issues if we are to progress.
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              Oxidative Stress and Epilepsy: Literature Review

              Backgrounds. The production of free radicals has a role in the regulation of biological function, cellular damage, and the pathogenesis of central nervous system conditions. Epilepsy is a highly prevalent serious brain disorder, and oxidative stress is regarded as a possible mechanism involved in epileptogenesis. Experimental studies suggest that oxidative stress is a contributing factor to the onset and evolution of epilepsy. Objective. A review was conducted to investigate the link between oxidative stress and seizures, and oxidative stress and age as risk factors for epilepsy. The role of oxidative stress in seizure induction and propagation is also discussed. Results/Conclusions. Oxidative stress and mitochondrial dysfunction are involved in neuronal death and seizures. There is evidence that suggests that antioxidant therapy may reduce lesions induced by oxidative free radicals in some animal seizure models. Studies have demonstrated that mitochondrial dysfunction is associated with chronic oxidative stress and may have an essential role in the epileptogenesis process; however, few studies have shown an established link between oxidative stress, seizures, and age.
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                Author and article information

                Journal
                Neuropsychiatr Dis Treat
                Neuropsychiatr Dis Treat
                Neuropsychiatric Disease and Treatment
                Neuropsychiatric Disease and Treatment
                Dove Medical Press
                1176-6328
                1178-2021
                2016
                22 April 2016
                : 12
                : 1013-1017
                Affiliations
                Department of Neurology, Dicle University, Diyarbakır, Turkey
                Author notes
                Correspondence: Mehmet Uğur Çevik, Department of Neurology, Dicle University, Sur, Diyarbakır, 21280, Turkey, Tel +90 412 248 8016, Fax +90 412 248 8523, Email mehmetugur.cevik@ 123456gmail.com
                Article
                ndt-12-1013
                10.2147/NDT.S103336
                4854258
                27175078
                f33574b1-395b-423f-9070-5a8944417440
                © 2016 Dönmezdil et al. This work is published and licensed by Dove Medical Press Limited

                The full terms of this license are available at https://www.dovepress.com/terms.php and incorporate the Creative Commons Attribution – Non Commercial (unported, v3.0) License ( http://creativecommons.org/licenses/by-nc/3.0/). By accessing the work you hereby accept the Terms. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed.

                History
                Categories
                Original Research

                Neurology
                epilepsy,paraoxonase 1,malondialdehyde,oxidative stress,biochemical marker
                Neurology
                epilepsy, paraoxonase 1, malondialdehyde, oxidative stress, biochemical marker

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