Methylphenidate treatment induces oxidative stress in young rat brain

Martins, Márcio Rodrigo; Reinke, Adalisa; Petronilho, Fabrícia; Gomes, Karin Martins; Dal‐Pizzol, Felipe; Quevedo, Joao L De

doi:10.1016/j.brainres.2006.01.004

Cited by 88 publications

(62 citation statements)

References 74 publications

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“…The inhibition of complex I caused by MPH may be related to the findings reported by Martins et al [62], which showed that MPH administration induced oxidative stress in the brain of young rats. Augmented ROS production induces lipoperoxidation and protein oxidative damage.…”

Section: Discussionsupporting

confidence: 73%

Effect of Acute and Chronic Administration of Methylphenidate on Mitochondrial Respiratory Chain in the Brain of Young Rats

Fagundes

Aguiar

et al. 2010

Neurochem Res

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Methylphenidate is commonly used for the treatment of attention deficit/hyperactivity disorder. There are still few works regarding the effects of methylphenidate on brain energy metabolism. Thus, in the present study we evaluated the effect of chronic administration of methylphenidate on the activities of mitochondrial respiratory chain complexes I and III in the brain of young rats. The effect of acute administration of methylphenidate on mitochondrial respiratory chain complexes I, II, III and IV in the brain of young rats was also investigated. For acute administration, a single injection of methylphenidate was given to rats on postnatal day 25. For chronic administration, methylphenidate injections were given starting at postnatal day 25 once daily for 28 days. Our results showed that complexes I and III were not affected by chronic administration of methylphenidate. Moreover, the acute administration of methylphenidate decreased complex I activity in cerebellum and prefrontal cortex, whereas complexes II, III and IV were not altered.

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Section: Discussionsupporting

confidence: 73%

Effect of Acute and Chronic Administration of Methylphenidate on Mitochondrial Respiratory Chain in the Brain of Young Rats

Fagundes

Aguiar

et al. 2010

Neurochem Res

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“…In other areas evaluated, the CAT activity was not altered following the any treatment with MPH in young or adult rats. Our group has shown that oxidative damage induced by MPH depends on the dose used, the period of exposure to drug, developmental period in that the exposure occur and the brain areas affected in rat [14]. By the way, the current observed results demonstrate that CAT and SOD activities augmented after MPH treatment, in young rat brain can contribute to oxidative stress formation, because those activities was not enough to prevent the free radicals generation.…”

Section: Discussionmentioning

confidence: 56%

“…The activity of SOD or CAT, but probably is not enough to prevent the oxidative damage in rat brain induced by MPH, since we have observed in another studies the increased mitochondrial respiratory chain enzymes that could increase oxidative stress following exposure [14,15]. Further studies would be necessary to clarify of the neurobiological effects of MPH associated with oxidative system.…”

Section: Discussionmentioning

confidence: 82%

“…The rationale for concern is compelling, since, in children, the CNS continues its maturation and growth well into the second decade of life [13]. Previously, our group showed that chronic exposure to MPH during early developmental induces oxidative damage and increase mitochondrial respiratory chain enzymes in young rat brain, deferentially from chronic exposure during adulthood [14,15]. However studies assessing the effects of MPH in the antioxidants enzymes activities have not been known.…”

Section: Introductionmentioning

confidence: 99%

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Antioxidant Enzyme Activities Following Acute or Chronic Methylphenidate Treatment in Young Rats

et al. 2007

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Methylphenidate (MPH) is psychostimulants used to treat Attention-Deficit/Hyperactivity Disorder and can lead to a long-lasting neurochemical and behavioral adaptations in experimental animals. In the present study, the cerebral antioxidant enzymatic system, superoxide dismutase (SOD) and catalase (CAT) was evaluated at in different age following MPH (1, 2 or 10 mg/kg MPH, i.p.) treatment in young rats. In the acute treatment the SOD activity decreased in the cerebral prefrontal cortex with opposite effect in the cerebral cortex; and the CAT activity decreased in hippocampus. In the chronic treatment the SOD activity increased in the hippocampus and cerebral cortex and decreased in the striatum. The observed changes on the enzyme activities in rat brain were dependent on the structure brain region and duration of treatment with MPH. Probably, the activity of enzymes was not be enough to prevent MPH-induced oxidative damage in specific regions from brain, such as observed for us in another recent study.

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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: 63%

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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Methylphenidate treatment induces oxidative stress in young rat brain

Cited by 88 publications

References 74 publications

Effect of Acute and Chronic Administration of Methylphenidate on Mitochondrial Respiratory Chain in the Brain of Young Rats

Effect of Acute and Chronic Administration of Methylphenidate on Mitochondrial Respiratory Chain in the Brain of Young Rats

Antioxidant Enzyme Activities Following Acute or Chronic Methylphenidate Treatment in Young Rats

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

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