Oxidative Damage and Schizophrenia: The Potential Benefit by Atypical Antipsychotics

Dakhale, Ganesh N.; Khanzode, Suchet D.; Khanzode, Shruti; Saoji, Anand; Khobragade, Linesh; Turankar, Avinash Vikram

doi:10.1159/000077368

Cited by 105 publications

(73 citation statements)

References 58 publications

(35 reference statements)

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“…Although the current state of evidence is not yet mature enough to adopt this in clinical practice, findings of syndrome- (Reddy et al, 2003) and phase-specific profiles, and treatment-related normalization (Bilici et al, 2001;Dakhale et al, 2004;Frey et al, 2007;Gergerlioglu et al, 2007;Henneman and Altschule, 1951;Herken et al, 2007;Khanzode et al, 2003;Ozcan et al, 2004;Zhang et al, 2003) support this as a possible future application. Genetic polymorphisms of antioxidant enzymes, associated with psychiatric disorders (Akyol et al, 2005;Saadat et al, 2007;Tosic et al, 2006), may have potential in assisting the identification of at-risk individuals.…”

Section: Discussionmentioning

confidence: 99%

“…Abnormalities in levels of antioxidants and oxidative products have been reported to reverse over the course of treatment with atypical antipsychotics, coinciding with symptomatic improvement (Dakhale et al, 2004;Zhang et al, 2003). In two published studies, baseline serum SOD (Dakhale et al, 2004;Zhang et al, 2003), MDA and ascorbic acid (Dakhale et al, 2004) levels in patients with schizophrenia significantly differed from those in age-and sex-matched controls, taking smoking status into consideration. Within the patient groups, their baseline levels significantly shifted towards normality after treatment with atypical antipsychotics over the study durations of 8 wk (Dakhale et al, 2004) and 12 wk (Zhang et al, 2003), respectively.…”

Section: Clinical Studiesmentioning

confidence: 99%

“…A concomitant reduction in GSH : GSSG ratio, inverse correlations between age and GSSG and between age and GR, as well as the loss of normal correlations that exist in ; 82 (Zoroglu et al, 2002) ; 46 ; 20 (Taneli et al, 2004) (Herken et al, 2001) ; 25 (Kuloglu et al, 2002c) Unchanged 50 (Abdalla et al, 1986) Decreased 48 (Altuntas et al, 2000) ; 31 (Ranjekar et al, 2003) ; 46 (Yao et al, 1998a) Assays of oxidative products TBARS/MDA Plasma Increased 26 (Mahadik et al, 1998) ; 100 ; 25 (Kuloglu et al, 2002c) ; 92 (Zhang et al, 2006a) ; 47 (Dietrich-Muszalska and Olas, 2007) ; 60 (Ben Othmen et al, 2007) Unchanged 31 (Ranjekar et al, 2003 (Zhang et al, 2003) ; 16 (Evans et al, 2003) ; 48 (Dakhale et al, 2004) No reversal of oxidants, antioxidants¡MDA with treatment 20 (Taneli et al, 2004) ; 40 (Sarandol et al, 2007a) Preclinical studies Rats Reversal of haloperidolinduced oxidative stress Clozapine, olanzapine, risperidone (Pillai et al, 2007) In-vitro cell studies Reversal of induced oxidative stress…”

Section: Assays Of Oxidants and Antioxidantsmentioning

confidence: 99%

“…In two published studies, baseline serum SOD (Dakhale et al, 2004;Zhang et al, 2003), MDA and ascorbic acid (Dakhale et al, 2004) levels in patients with schizophrenia significantly differed from those in age-and sex-matched controls, taking smoking status into consideration. Within the patient groups, their baseline levels significantly shifted towards normality after treatment with atypical antipsychotics over the study durations of 8 wk (Dakhale et al, 2004) and 12 wk (Zhang et al, 2003), respectively. Another study with a smaller sample size conducted over 6 months likewise showed normalization of the antioxidative enzymes SOD, CAT and GSH-Px with treatment (Evans et al, 2003).…”

Section: Clinical Studiesmentioning

confidence: 99%

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Oxidative stress in psychiatric disorders: evidence base and therapeutic implications

Berk

Dean

et al. 2008

Int. J. Neuropsychopharm.

861

569

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Oxidative stress has been implicated in the pathogenesis of diverse disease states, and may be a common pathogenic mechanism underlying many major psychiatric disorders, as the brain has comparatively greater vulnerability to oxidative damage. This review aims to examine the current evidence for the role of oxidative stress in psychiatric disorders, and its academic and clinical implications. A literature search was conducted using the Medline, Pubmed, PsycINFO, CINAHL PLUS, BIOSIS Previews, and Cochrane databases, with a time-frame extending to September 2007. The broadest data for oxidative stress mechanisms have been derived from studies conducted in schizophrenia, where evidence is available from different areas of oxidative research, including oxidative marker assays, psychopharmacology studies, and clinical trials of antioxidants. For bipolar disorder and depression, a solid foundation for oxidative stress hypotheses has been provided by biochemical, genetic, pharmacological, preclinical therapeutic studies and one clinical trial. Oxidative pathophysiology in anxiety disorders is strongly supported by animal models, and also by human biochemical data. Pilot studies have suggested efficacy of N-acetylcysteine in cocaine dependence, while early evidence is accumulating for oxidative mechanisms in autism and attention deficit hyperactivity disorder. In conclusion, multi-dimensional data support the role of oxidative stress in diverse psychiatric disorders. These data not only suggest that oxidative mechanisms may form unifying common pathogenic pathways in psychiatric disorders, but also introduce new targets for the development of therapeutic interventions.

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Section: Discussionmentioning

confidence: 99%

Section: Clinical Studiesmentioning

confidence: 99%

Section: Assays Of Oxidants and Antioxidantsmentioning

confidence: 99%

Section: Clinical Studiesmentioning

confidence: 99%

See 2 more Smart Citations

Oxidative stress in psychiatric disorders: evidence base and therapeutic implications

Berk

Dean

et al. 2008

Int. J. Neuropsychopharm.

861

569

View full text Add to dashboard Cite

show abstract

“…16 The levels of SOD have been consistently found to be high in chronic schizophrenia patients 46 or low in neuroleptic naïve first-episode patients. 31 The vulnerability of striatal neurons to excitatory neurotransmission was exacerbated by neuroleptics, 47 suggesting elevated SOD levels and activity may be in part attributed to neuroleptics. However, neuroleptics acting at dopamine D2 receptors augment the synaptic release of glutamate, resulting in neural degeneration and increased production of oxyradicals thereby causing expression and/or activity of SOD to increase.…”

Section: Metabolismmentioning

confidence: 99%

A proteome analysis of the anterior cingulate cortex gray matter in schizophrenia

et al. 2006

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The Anterior Cingulate Cortex (ACC, Brodmans Area 24) is implicated in the pathogenesis of schizophrenia due to its normal functions and connectivity together with reports of structural, morphological and neurotransmitter aberrations within this brain area in the disease state. Two-dimensional gel electrophoresis (2DE) was employed to scan and compare the ACC gray matter proteomes between schizophrenia (n = 10) and control (n = 10) post-mortem human tissue. This proteomic approach has detected 42 protein spots with altered levels in the schizophrenia cohort, which to our knowledge is the first proteomic analysis of the ACC in schizophrenia. Thirty nine of these proteins were subsequently identified using mass spectrometry and functionally classified into metabolism and oxidative stress, cytoskeletal, synaptic, signalling, trafficking and glial-specific groups. Some of the identified proteins have previously been implicated in the disease pathogenesis and some offer new insights into schizophrenia. Investigating these proteins, the genes encoding these proteins, their functions and interactions may shed light on the molecular mechanisms underlying the heterogeneous symptoms characteristic of schizophrenia.

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Current awareness in human psychopharmacology

2004

Human Psychopharmacology

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In order to keep subscribers up‐to‐date with the latest developments in their field, John Wiley & Sons are providing a current awareness service in each issue of the journal. The bibliography contains newly published material in the field of human psychopharmacology. Each bibliography is divided into 18 sections: 1 Books, Reviews & Symposia; 2 General; 3 Psychotropic Drugs ‐ General; Antidepressive Agents: 4 Tricyclics; 5 Monoamine Oxidase Inhibitors; 6 Serotonergics; Euthymic Agents: 7 Lithium; Tranquillizing Agents: 8 Major; 9 Minor & Hypnotics; 10 Analeptic Agents; 11 Anticonvulsant Agents; 12 Drugs of Abuse; 13 Transmitters, Receptors, Metabolites & Modulating Agents; 14 Neuropeptides; 15 Psychoneuroendocrinology; 16 Psychoneuroimmunology; 17 Behavioural Genetics; 18 Others. Within each section, articles are listed in alphabetical order with respect to author. If, in the preceding period, no publications are located relevant to any one of these headings, that section will be omitted.

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Oxidative Damage and Schizophrenia: The Potential Benefit by Atypical Antipsychotics

Cited by 105 publications

References 58 publications

Oxidative stress in psychiatric disorders: evidence base and therapeutic implications

Oxidative stress in psychiatric disorders: evidence base and therapeutic implications

A proteome analysis of the anterior cingulate cortex gray matter in schizophrenia

Current awareness in human psychopharmacology

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