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      Dynamic Thiol/Disulfide Homeostasis and Oxidative DNA Damage in Adult Attention Deficit Hyperactivity Disorder

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          Abstract

          Objective

          Insufficient number of oxidative stress studies have been conducted in patients with adult attention deficit hyperactivity disorder (ADHD). The objective of the current study is to examine the thiol/disulfide homeostasis as well as oxidative DNA damage levels in adult ADHD patients and to compare them with the results of healthy control subjects.

          Methods

          The study was inclusive of forty-nine patients who were diagnosed with adult ADHD, as well as thirty-three healthy volunteers to be used as the control group. The diagnosis of the patients was conducted according to the DSM-5 diagnostic criteria. Blood were stored under appropriate laboratory conditions. For the purpose of detecting the oxidative DNA damage level, an extraction of genomic DNA from leukocytes was carried out, and furthermore the levels of 8-hydroxy-2-deoxyguanosine (8-OHdG), apart from deoxyguanosine, were measured accordingly.

          Results

          Total thiol and the native thiol levels were observed to be statistically lower in adult ADHD patients as compared to the subjects in the healthy control group ( p = 0.001). It was observed that the disulfide levels were higher in adult ADHD patients as compared to the healthy control subjects ( p = 0.001). In addition, the levels of 8-OHdG, which are considered as a marker for assessing DNA damage, were found to be significantly lower in the control group as compared to the adult ADHD patients ( p = 0.001).

          Conclusion

          It was observed that the thiol/disulfide homeostasis had shifted towards disulfide, and 8-OHdG levels were increased in adult ADHD patients.

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          Most cited references48

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          Free radicals, metals and antioxidants in oxidative stress-induced cancer.

          Oxygen-free radicals, more generally known as reactive oxygen species (ROS) along with reactive nitrogen species (RNS) are well recognised for playing a dual role as both deleterious and beneficial species. The "two-faced" character of ROS is substantiated by growing body of evidence that ROS within cells act as secondary messengers in intracellular signalling cascades, which induce and maintain the oncogenic phenotype of cancer cells, however, ROS can also induce cellular senescence and apoptosis and can therefore function as anti-tumourigenic species. The cumulative production of ROS/RNS through either endogenous or exogenous insults is termed oxidative stress and is common for many types of cancer cell that are linked with altered redox regulation of cellular signalling pathways. Oxidative stress induces a cellular redox imbalance which has been found to be present in various cancer cells compared with normal cells; the redox imbalance thus may be related to oncogenic stimulation. DNA mutation is a critical step in carcinogenesis and elevated levels of oxidative DNA lesions (8-OH-G) have been noted in various tumours, strongly implicating such damage in the etiology of cancer. It appears that the DNA damage is predominantly linked with the initiation process. This review examines the evidence for involvement of the oxidative stress in the carcinogenesis process. Attention is focused on structural, chemical and biochemical aspects of free radicals, the endogenous and exogenous sources of their generation, the metal (iron, copper, chromium, cobalt, vanadium, cadmium, arsenic, nickel)-mediated formation of free radicals (e.g. Fenton chemistry), the DNA damage (both mitochondrial and nuclear), the damage to lipids and proteins by free radicals, the phenomenon of oxidative stress, cancer and the redox environment of a cell, the mechanisms of carcinogenesis and the role of signalling cascades by ROS; in particular, ROS activation of AP-1 (activator protein) and NF-kappaB (nuclear factor kappa B) signal transduction pathways, which in turn lead to the transcription of genes involved in cell growth regulatory pathways. The role of enzymatic (superoxide dismutase (Cu, Zn-SOD, Mn-SOD), catalase, glutathione peroxidase) and non-enzymatic antioxidants (Vitamin C, Vitamin E, carotenoids, thiol antioxidants (glutathione, thioredoxin and lipoic acid), flavonoids, selenium and others) in the process of carcinogenesis as well as the antioxidant interactions with various regulatory factors, including Ref-1, NF-kappaB, AP-1 are also reviewed.
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            Reactive oxygen species, cellular redox systems, and apoptosis.

            Reactive oxygen species (ROS) are products of normal metabolism and xenobiotic exposure, and depending on their concentration, ROS can be beneficial or harmful to cells and tissues. At physiological low levels, ROS function as "redox messengers" in intracellular signaling and regulation, whereas excess ROS induce oxidative modification of cellular macromolecules, inhibit protein function, and promote cell death. Additionally, various redox systems, such as the glutathione, thioredoxin, and pyridine nucleotide redox couples, participate in cell signaling and modulation of cell function, including apoptotic cell death. Cell apoptosis is initiated by extracellular and intracellular signals via two main pathways, the death receptor- and the mitochondria-mediated pathways. Various pathologies can result from oxidative stress-induced apoptotic signaling that is consequent to ROS increases and/or antioxidant decreases, disruption of intracellular redox homeostasis, and irreversible oxidative modifications of lipid, protein, or DNA. In this review, we focus on several key aspects of ROS and redox mechanisms in apoptotic signaling and highlight the gaps in knowledge and potential avenues for further investigation. A full understanding of the redox control of apoptotic initiation and execution could underpin the development of therapeutic interventions targeted at oxidative stress-associated disorders. Copyright 2010 Elsevier Inc. All rights reserved.
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              Clinical Practice Guideline for the Diagnosis, Evaluation, and Treatment of Attention-Deficit/Hyperactivity Disorder in Children and Adolescents

              Attention-deficit/hyperactivity disorder (ADHD) is 1 of the most common neurobehavioral disorders of childhood and can profoundly affect children's academic achievement, well-being, and social interactions. The American Academy of Pediatrics first published clinical recommendations for evaluation and diagnosis of pediatric ADHD in 2000; recommendations for treatment followed in 2001. The guidelines were revised in 2011 and published with an accompanying process of care algorithm (PoCA) providing discrete and manageable steps by which clinicians could fulfill the clinical guideline's recommendations. Since the release of the 2011 guideline, the Diagnostic and Statistical Manual of Mental Disorders has been revised to the fifth edition, and new ADHD-related research has been published. These publications do not support dramatic changes to the previous recommendations. Therefore, only incremental updates have been made in this guideline revision, including the addition of a key action statement related to diagnosis and treatment of comorbid conditions in children and adolescents with ADHD. The accompanying process of care algorithm has also been updated to assist in implementing the guideline recommendations. Throughout the process of revising the guideline and algorithm, numerous systemic barriers were identified that restrict and/or hamper pediatric clinicians' ability to adopt their recommendations. Therefore, the subcommittee created a companion article (available in the Supplemental Information) on systemic barriers to the care of children and adolescents with ADHD, which identifies the major systemic-level barriers and presents recommendations to address those barriers; in this article, we support the recommendations of the clinical practice guideline and accompanying process of care algorithm.
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                Author and article information

                Journal
                Clin Psychopharmacol Neurosci
                Clin Psychopharmacol Neurosci
                Clinical Psychopharmacology and Neuroscience
                Korean College of Neuropsychopharmacology
                1738-1088
                2093-4327
                30 November 2021
                30 November 2021
                30 November 2021
                : 19
                : 4
                : 731-738
                Affiliations
                [1 ]Department of Psychiatry, Faculty of Medicine, Van Yuzuncu Yil University, Van, Turkey
                [2 ]Department of Biochemistry, Faculty of Medicine, Van Yuzuncu Yil University, Van, Turkey
                Author notes
                Address for correspondence: Faruk Kurhan Department of Psychiatry, Faculty of Medicine, Van Yuzuncu Yil University, Van 65100, Turkey, E-mail: fkurhan@ 123456hotmail.com , ORCID: https://orcid.org/0000-0003-3718-0458
                Author information
                https://orcid.org/0000-0003-3718-0458
                https://orcid.org/0000-0002-9202-4944
                Article
                cpn-19-4-731
                10.9758/cpn.2021.19.4.731
                8553522
                34690128
                9b85df00-3f1e-4e63-b5b3-b84ddc2da488
                Copyright© 2021, Korean College of Neuropsychopharmacology

                This is an open-access article distributed under the terms of the Creative Commons Attribution Non-Commercial License ( http://creativecommons.org/licenses/by-nc/4.0) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                : 4 January 2021
                : 2 February 2021
                : 5 February 2021
                Categories
                Original Article

                adult adhd,thiol disulfide,oxidative dna damage
                adult adhd, thiol disulfide, oxidative dna damage

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