Increased oxidative stress and oxidative DNA damage in non-remission schizophrenia patients

Çöpoğlu, Ümit Sertan; Virit, Osman; Kokaçya, Mehmet Hanifi; Örkmez, Mustafa; Bülbül, Feridun; Erbağcı, Ahmet; Sönmezer, Murat; Alpak, Gökay; Ünal, Ahmet; Arı, Mustafa; Savaş, Haluk A.

doi:10.1016/j.psychres.2015.07.036

Cited by 64 publications

(43 citation statements)

References 56 publications

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“…Consistent with evidence from other studies, our findings suggest brain oxidative stress and altered energy production in SZ. [9][10][11][33][34][35] Since RR can affect numerous critical enzymatic reactions, our findings for reduced RR in both FE and chronic SZ patients provide an important new insight into the pathophysiology of this major psychiatric condition.…”

Section: Discussionmentioning

confidence: 69%

“…Several lines of evidence suggest SZ is associated with a range of biochemical brain abnormalities, including mitochondrial dysfunction, 1-3 impaired bioenergetics, 4 neuroinflammation, [5][6][7][8] and oxidative stress. [9][10][11][12] Nicotinamide adenine dinucleotide (NAD), which exists in oxidized (NAD+) and reduced form (NADH) has long been implicated in energy metabolism, reductive biosynthesis, and antioxidant activity. While the major biological function of NAD+ is to modulate cellular energy metabolism, mounting evidence indicates that NAD+ is also involved in biological activities such as cell death, 13,14 calcium homeostasis, 15,16 gene expression, 17,18 aging, carcinogenesis, and immunological functions.…”

Section: Introductionmentioning

confidence: 99%

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Redox Dysregulation in Schizophrenia Revealed by in vivo NAD+/NADH Measurement

Kim

Cohen

Chen

et al. 2016

Schizophrenia Bulletin

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Balance between the redox pair of nicotinamide adenine dinucleotides (oxidized NAD+ and reduced NADH), reflects the oxidative state of cells and the ability of biological systems to carry out energy production. A growing body of evidence suggests that an "immuno-oxidative" pathway including oxidative stress, mitochondrial dysfunction, neuroinflammation, and cell-mediated immune response may contribute to disruptions in brain activity in schizophrenia (SZ). The aim of this study is to assess possible redox imbalance in SZ patients by using a novel in vivo 31 P MRS technique. The participants included 40 healthy controls, 21 chronic SZ, 13 first-episode (FE) SZ, and 18 FE bipolar disorder (BD) patients (as a psychiatric control group). All participants initially underwent structural imaging at a 3 Tesla (3 T) and 31 P MRS measurements were performed on a 4 T MR scanner. NAD+ and NADH components were determined by nonlinear least-square fitting of the model simulated spectra; these incorporated prior chemical shift and coupling constant information to in vivo resonances obtained from 31 P MRS experiments. We found a significant reduction in the NAD+/NADH ratio in chronically ill SZ patients compared to a matched healthy control group, and in FE SZ patients compared to both a matched FE BD patient group and a matched healthy control group. These findings provide evidence for redox imbalance in the brain in all phases of SZ, potentially reflecting oxidative stress.

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Section: Discussionmentioning

confidence: 69%

Section: Introductionmentioning

confidence: 99%

Redox Dysregulation in Schizophrenia Revealed by in vivo NAD+/NADH Measurement

Kim

Cohen

Chen

et al. 2016

Schizophrenia Bulletin

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“…(2013) found an increase in blood markers of lipid peroxidation (i.e., MDA and/or TBARS) in SZ, already present in first‐episode psychotic patients . However, in individual studies, 8‐OHdG was found to be increased in patients with non‐remitting schizophrenia although not in adolescents with a first psychotic episode, suggesting its association with a chronic disease course . In depression, Jiménez‐Fernández et al.…”

Section: Discussionmentioning

confidence: 99%

Oxidative and nitrosative stress markers in obsessive–compulsive disorder: a systematic review and meta‐analysis

Maia

Oliveira

Lajnef

et al. 2019

Acta Psychiatr Scand

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Oxidative and nitrosative stress markers in obsessive-compulsive disorder: a systematic review and meta-analysis Maia A, Oliveira J, Lajnef M, Mallet L, Tamouza R, Leboyer M, Oliveira-Maia AJ. Oxidative and nitrosative stress markers in obsessive-compulsive disorder: a systematic review and meta-analysis Objective: Obsessive-compulsive disorder (OCD) is a chronic, prevalent, and highly impairing psychiatric illness. Although the pathophysiology of OCD remains unknown, pathways involved in oxidative and nitrosative stress (O&NS) have been implicated. The present study aims to systematically review the literature for quantitative evidence that patients with OCD have altered measures of blood O&NS markers. Methods: Independent random-effects meta-analyses using standardized mean differences were conducted to assess each marker separately. Additionally, data from multiple markers were pooled together in a metaanalysis for measures of oxidant activity and another for measures of antioxidant activity. Results: Thirteen studies met inclusion criteria, involving 433 OCD patients and 459 controls. Eleven blood O&NS markers were eligible for independent quantitative analyses. We found that, in OCD patients, the oxidant markers 8-hydroxydeoxyguanosine and malondialdehyde, and the antioxidants glutathione peroxidase and superoxide dismutase, were significantly increased while total antioxidant status, vitamin C, and vitamin E were significantly decreased, when comparing with controls. Regarding pooled meta-analyses, we found a statistically significant increase in oxidant markers, but non-significant results regarding antioxidant markers. Conclusions: Our meta-analysis suggests that OCD patients have a systemic oxidative imbalance that is not adequately buffered by the antioxidant system. Additional studies are needed in order to support this association. Summations• Patients with obsessive-compulsive disorder have a dysregulated oxidative profile with increased blood oxidative markers.• No global changes in antioxidant defenses in obsessive-compulsive disorder are of remark thus suggesting that oxidative stress is not adequately buffered.• Our results underline the systemic impact of obsessive-compulsive disorder and should motivate the development of future studies in order to better understand this association. Considerations• Most studies did not provide measurements of oxidative and nitrosative stress markers according to pertinent demographic and clinical characteristics thus impairing relevant sensitivity analyses that would have allowed to assess the potential impact of these factors in the results.• The limited number of studies, their moderate quality and heterogeneity, and the evidence for publication bias prevent more robust conclusions.

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“…This alteration has been recognized in treated, untreated and early-stage schizophrenic patients (Boskovic et al 2011). For example, a higher level of 8-oxodG in the blood has been reported in non-remission schizophrenia patients (Sertan Copoglu et al 2015). Also, both urinary 8-oxodG and 8-oxoGuo levels were significantly increased in the schizophrenia patients (Jorgensen et al 2013a).…”

Section: Dna Damage In Schizophreniamentioning

confidence: 99%

“…These biomarkers have been commonly used to estimate the DNA damage in humans after exposure to cancer-causing agents, such as tobacco smoke, asbestos fibers, heavy metals, and polycyclic aromatic hydrocarbons. However, in recent years, 8-oxodG and 8-oxoGuo levels in the urine, blood and brain tissues have been widely used as not only an endogenous oxidative nucleotide damage biomarker (Evans et al 2004, Nishioka & Arnold 2004, Hu et al 2010, Sertan Copoglu et al 2015), but also as a risk factor for many diseases (Wei et al 2009). …”

Section: Dna Damage and Cellular Balance Between Oxidative Stress mentioning

confidence: 99%

DNA Damage in Major Psychiatric Diseases

et al. 2016

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Human cells are exposed to exogenous insults and continuous production of different metabolites. These insults and unwanted metabolic products might interfere with the stability of genomic DNA. Recently many studies demonstrated that different psychiatric disorders show substantially high level of oxidative DNA damage in the brain accompanied with morphological and functional alterations. It reveals that damaged genomic DNA may contribute to the pathophysiology of these mental illnesses. Here we review the role of oxidative damage and reduced antioxidant ability in some vastly studied psychiatric disorders and emphasize the inclusion of treatment options involving DNA repair. In addition, while most currently used antidepressants are based on the manipulation of the neurotransmitter regulation in managing different mental abnormalities, they are able to prevent or reverse neurotoxin-induced DNA damage. Therefore, it may be plausible to target on genomic DNA alterations for psychiatric therapies, which is of pivotal importance for future anti-psychiatric drug development.

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Increased oxidative stress and oxidative DNA damage in non-remission schizophrenia patients

Cited by 64 publications

References 56 publications

Redox Dysregulation in Schizophrenia Revealed by in vivo NAD+/NADH Measurement

Redox Dysregulation in Schizophrenia Revealed by in vivo NAD+/NADH Measurement

Oxidative and nitrosative stress markers in obsessive–compulsive disorder: a systematic review and meta‐analysis

DNA Damage in Major Psychiatric Diseases

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