Attention Deficit Hyperactivity Disorder and oxidative stress: A short term follow up study

Güney, Esra; Çetin, Fatih Hilmi; Alışık, Murat; Tunca, Hüseyin; Torun, Yasemin Taş; İşeri, Elvan; Taner, Yasemen; Çayci, Banu; Erel, Özcan

doi:10.1016/j.psychres.2015.07.003

Cited by 52 publications

(41 citation statements)

References 37 publications

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“…For sulfhydryl groups, the data are very limited. It has only been reported that sulfhydryl levels were significantly higher in children and adolescent ADHD patients than in control patients (Guney et al 2015). A direct relationship between oxidative stress and ADHD was reported by Bulut et al (2007), Oztop et al (2012) and Sezen et al (2016).…”

Section: Discussionmentioning

confidence: 99%

ADHD pathogenesis in the immune, endocrine and nervous systems of juvenile and maturating SHR and WKY rats

et al. 2019

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RationaleAttention-deficit/hyperactivity disorder (ADHD) is one of the most common neurobehavioural disorders with morphological and functional brain abnormalities. However, there is a growing body of evidence that abnormalities in the immune and endocrine systems may also account for the ADHD pathogenesis.ObjectivesTo test ADHD pathogenesis in neurological, immune and endocrine systems, this study examined the concentrations of cytokines, chemokines, oxidative stress markers, metabolic parameters, steroid hormones and steroidogenic enzymes in the serum and/or tissues of spontaneously hypertensive rats (SHRs, animal model of ADHD) and Wistar Kyoto rats (WKYs, control animals). Moreover, the volume of the medial prefrontal cortex (mPFC) as well as the density of dopamine 2 (D2) receptor-expressing cells and tyrosine hydroxylase (TH)-positive nerve fibres in it was also elucidated.MethodsPeripheral blood, spleen and adrenal gland samples, as well as brain sections collected on day 35 (juvenile) and day 70 (maturating) from SHRs and WKYs, were processed by ELISA and immunohistochemistry, respectively.ResultsThe results show significant increases of serum and/or tissue concentrations of cytokines, chemokines and oxidative stress markers in juvenile SHRs when compared to the age-matched WKYs. These increases were accompanied by a lowered volume of the mPFC and up-regulation of D2 in this brain region. In maturating SHRs, the levels of inflammatory and oxidative stress markers were normalised and accompanied by elevated contents of steroid hormones.ConclusionsSignificant elevations of serum and/or tissue contents of cytokines, chemokines and oxidative stress markers as well as volumetric and neurochemical alterations in the mPFC of juvenile SHRs may suggest the cooperation of neurological and immune systems in the ADHD pathogenesis. Elevated levels of steroid hormones in maturating SHRs may be a compensatory effect involved in reducing inflammation and ADHD symptoms.

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Section: Discussionmentioning

confidence: 99%

ADHD pathogenesis in the immune, endocrine and nervous systems of juvenile and maturating SHR and WKY rats

et al. 2019

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“…In one another study one group investigated total antioxidative status and total oxidative status of plasma and antioxidant enzyme. Oxidative stress index values and the plasma TOS levels of the patients with ADHD were statistically higher than those of the control group [25]. Sezen et al [26] also investigated and found that oxidative stress was higher in the ADHD patients than the control group.…”

Section: Discussionmentioning

confidence: 96%

Attention deficit-hyperactivity disorder suffers from mitochondrial dysfunction

et al. 2016

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BackgroundPathophysiology of attention-deficit hyperactivity disorder (ADHD) is not known, and therefore the present study investigated mitochondrial defects, if any in cybrids created from patients and control population.MethodsTo investigate mitochondrial pathology in ADHD, cybrids cell lines were created from ADHD probands and controls by fusing their platelets with ρ0-cells prepared from SH-SY5Y neuroblastoma cell line. Cellular respiration, oxidative stress, mitochondrial membrane potential and morphology were evaluated employing oxygraph, mitochondria-specific fluorescence staining and evaluation by FACS, and immunocytochemistry. HPLC-electrochemical detection, quantitative RT-PCR and Blue Native PAGE were employed respectively for assays of serotonin, mitochondrial ATPase 6/8 subunits levels and complex V activity.ResultsSignificantly low cellular and mitochondrial respiration, ATPase6/8 transcripts levels, mitochondrial complex V activity and loss of mitochondrial membrane potential and elevated oxidative stress were observed in ADHD cybrids. Expression of monoamine oxidizing mitochondrial enzymes, MAO-A and MAO-B levels remained unaffected. Two-fold increase in serotonin level was noted in differentiated cybrid-neurons.ConclusionsSince cybrids are shown to replicate mitochondrial defects seen in post-mortem brains, these observed defects in ADHD cybrids strongly suggest mitochondrial pathology in this disorder.General significanceMitochondrial defects are detected in ADHD cybrids created from patients' platelets, implying bioenergetics crisis in the mitochondria could be a contributory factor for ADHD pathology and/or phenotypes.

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“…In fact, it was shown that MPH triggers ROS production in various animal studies [60,61]. By contrast, a clinical study points to protective effects of MPH against oxidative stress, at least after 12 weeks of MPH medication [62]. All NOS isoforms including eNOS can produce both NO and superoxide [63].…”

Section: Blood Pressure In Pediatric Adhd and Potential Effects Of Mphmentioning

confidence: 99%

Enhanced Nitric Oxide (NO) and Decreased ADMA Synthesis in Pediatric ADHD and Selective Potentiation of NO Synthesis by Methylphenidate

Jansen

Hanusch

Pross

et al. 2020

JCM

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Attention deficit hyperactivity disorder (ADHD) is a common pediatric psychiatric disorder, frequently treated with methylphenidate (MPH). Recently, MPH’s cardiovascular safety has been questioned by observational studies describing an increased cardiovascular risk in adults and blood pressure alterations in children. We considered members of the L-arginine (Arg)/nitric oxide (NO) pathway as possible early cardiovascular risk factors in pediatric ADHD children. They include the NO metabolites, nitrite and nitrate, the NO precursor Arg, and asymmetric dimethylarginine (ADMA), an endogenous NO synthase (NOS) inhibitor and a cardiovascular risk factor in adults. We conducted a prospective clinical trial with 42 ADHD children (aged 6–16 years) with (n = 19) and without (n = 23) MPH treatment. Age-matched children without ADHD (n = 43) served as controls. All plasma and urine metabolites were determined by gas chromatography-mass spectrometry. We observed higher plasma nitrite and lower plasma ADMA concentrations in the ADHD children. MPH-treated ADHD children had higher plasma nitrite concentrations than MPH-untreated ADHD children. As NOS activity is basally inhibited by ADMA, MPH treatment seems to have decreased the inhibitory potency of ADMA. Percentiles of systolic blood pressure were higher in MPH-treated ADHD children. The underlying mechanisms and their implications in the MPH therapy of pediatric ADHD with MPH remain to be elucidated in larger cohorts.

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Attention Deficit Hyperactivity Disorder and oxidative stress: A short term follow up study

Cited by 52 publications

References 37 publications

ADHD pathogenesis in the immune, endocrine and nervous systems of juvenile and maturating SHR and WKY rats

ADHD pathogenesis in the immune, endocrine and nervous systems of juvenile and maturating SHR and WKY rats

Attention deficit-hyperactivity disorder suffers from mitochondrial dysfunction

Enhanced Nitric Oxide (NO) and Decreased ADMA Synthesis in Pediatric ADHD and Selective Potentiation of NO Synthesis by Methylphenidate

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