Methylphenidate treatment causes oxidative stress and alters energetic metabolism in an animal model of attention-deficit hyperactivity disorder

Comim, Clarissa M.; Gomes, Karin Martins; Réus, Gislaine Z.; Petronilho, Fabrícia; Ferreira, Gabriela K.; Streck, Emílio L.; Dal‐Pizzol, Felipe; Quevedo, João

doi:10.1017/neu.2013.35

Cited by 34 publications

(30 citation statements)

References 48 publications

(53 reference statements)

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“…Findings are inconsistent with reports of positive (Schmidt et al 2010;Schmitz et al 2012a), adverse (Comim et al 2014;Martins et al 2006;Schmitz et al 2012b) and null effects (Cöngöloğlu et al 2006;Gomes et al 2008). This makes conclusions about the impact of such medications on O&NS difficult as results seem to be influenced by treatment duration (acute versus chronic), age of population (young versus adult), brain region examined, biomarker measured, and dosage of drug administered.…”

Section: Potential Causes Of Oandns In Adhdmentioning

confidence: 62%

Oxidative and nitrosative stress in ADHD: possible causes and the potential of antioxidant-targeted therapies

Lopresti

2015

ADHD Atten Def Hyp Disord

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Attention deficit hyperactivity disorder (ADHD) has a complex etiology although theories associated with disturbances in dopaminergic and noradrenergic activity are most commonly cited.The importance of these catecholamines in ADHD is supported by its effective treatment utilising stimulant and non-stimulant medications that modify their activity. Recently there has been interest in oxidative and nitrosative stress (O&NS) in ADHD and its potential to contribute to this condition. In this article, research investigating O&NS in ADHD is reviewed and its impact on catecholaminergic activity and neurological structure is discussed. Lifestyle, environmental, ADHD is most commonly treated with stimulant medications such as methylphenidate and amphetamines, non-stimulants such as atomoxetine, and alpha2-adrenergic agonists such as clonidine and guanfacine. Through their effects on dopamine and noradrenaline transporters, stimulants inhibit the reuptake of dopamine and noradrenaline, thereby increasing the extracellular levels of these neurotransmitters. These stimulants also inhibit monoamine oxidase, the enzyme that metabolises these catecholamines (Wilens et al. 2011). Atomoxetine works as a selective reuptake inhibitor of noradrenaline leading to its increased extracellular concentration (Garnock- Jones and Keating 2009).While effective, these medications are associated with several adverse effects. These include loss of appetite, growth delay and sleep disturbances (Cortese et al. 2013). It is important to note that despite their widely accepted short-term efficacy, the long-term effectiveness of pharmacological treatments on social, educational and occupational functioning in people with ADHD continues to be debated (Huang and Tsai 2011;Langberg and Becker 2012;Nijmeijer et al. 2008). On a positive note, recent analyses using the Swedish national registrar suggests that long-term stimulant use in people with ADHD is associated with reduced rates of substance use, criminality, and serious traffic accidents (Chang et al. 2014a;Chang et al. 2014b;Lichtenstein et al. 2012).Despite wide appreciation of catecholaminergic theories associated with ADHD, there has been increased research into other biological mechanisms associated with ADHD. For example, in psychiatry there has been interest in immune-inflammatory pathways and oxidative and nitrosative stress (O&NS). In particular, it has been confirmed through recent meta-analyses that depression is Increased O&NS has also been found in bipolar disorder (Andreazza et al. 2008;Brown et al. 2014),

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Section: Potential Causes Of Oandns In Adhdmentioning

confidence: 62%

Oxidative and nitrosative stress in ADHD: possible causes and the potential of antioxidant-targeted therapies

Lopresti

2015

ADHD Atten Def Hyp Disord

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“…Furthermore, MPH undermines both enzymatic and non-enzymatic antioxidant defense systems in some parts of brain [5]. MPH and other methamphetamine like compounds have been observed to ameliorate the brain GSH content while decreasing the hippocampal antioxidant activities such as SOD, GPx and GR.…”

Section: Discussionmentioning

confidence: 99%

“…The doses of MPH were selected according to our pilot study and previous studies. Multiple protocols for duration of treatment were used previously, we decided to investigate the effects of chronic doses of MPH for 21 days on adult rats based on similar studies [5,26].…”

Section: Experimental Designmentioning

confidence: 99%

Effects of chronic treatment with methylphenidate on oxidative stress and inflammation in hippocampus of adult rats

Motaghinejad

Motevalian

Shabab

2016

Neuroscience Letters

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“…Most important in this regard is methylphenidate. As with cocaine, there are reports of increased oxidative stress and lipid peroxidation in certain brain regions after methylphenidate, whereas long-term depletion of monoamine levels is not observed (Yuan et al, 1997;Schmitz et al, 2012;Comim et al, 2014). Analogous with cocaine, methylphenidate also protects against toxicity of amphetamines, and it has been suggested it may also be protective against the neurodegenerative processes occurring in Parkinson's disease (Volz, 2008).…”

Section: Drug-induced Neuroplasticitymentioning

confidence: 99%

Mechanisms of Action and Persistent Neuroplasticity by Drugs of Abuse

Korpi¹,

Hollander²,

Farooq

et al. 2015

Pharmacol Rev

123

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Methylphenidate treatment causes oxidative stress and alters energetic metabolism in an animal model of attention-deficit hyperactivity disorder

Cited by 34 publications

References 48 publications

Oxidative and nitrosative stress in ADHD: possible causes and the potential of antioxidant-targeted therapies

Oxidative and nitrosative stress in ADHD: possible causes and the potential of antioxidant-targeted therapies

Effects of chronic treatment with methylphenidate on oxidative stress and inflammation in hippocampus of adult rats

Mechanisms of Action and Persistent Neuroplasticity by Drugs of Abuse

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