The Role of Nitric Oxide and Nitrosative Stress in Schizophrenia

Dietrich‐Muszalska, Anna; Bartosz, Grzegorz; Sadowska-Bartosz, Izabela

doi:10.1007/978-1-4939-0440-2_15

Cited by 3 publications

(2 citation statements)

References 146 publications

(142 reference statements)

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“…Peroxynitrite causes mainly nitration of tyrosine residue in proteins to form 3-nitrotyrosine (3-NT) – marker of nitrative stress. 45 The level of NO metabolites was found to be significantly higher in platelets of patients treated with AADs than in platelets of control subjects. 46 Increased protein nitration, as measured by the level of 3-NT, was observed in the prefrontal cortex of schizophrenic patients.…”

Section: Discussionmentioning

confidence: 90%

“…Nitric oxide (NO) produced in brain mainly enzymatically by NOS (nitric oxide synthase) is involved in brain functioning and may play a dual role, both neuroprotective and neurotoxic. 45 Its reaction with superoxide radical and formation of peroxynitrite leads to damaging effects. Peroxynitrite reacts with different biological molecules, damaging proteins, nucleic acids, initiating lipid peroxidation in membranes of the cells.…”

Section: Discussionmentioning

confidence: 99%

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Comparative Study of the Effects of Atypical Antipsychotic Drugs on Plasma and Urine Biomarkers of Oxidative Stress in Schizophrenic Patients

Dietrich‐Muszalska¹,

Kołodziejczyk-Czepas²,

Nowak³

2021

NDT

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Purpose Evidence that antipsychotic drugs (ADs) can affect oxidative stress estimated with various biomarkers in schizophrenic patients is controversial and limited. Therefore, in the present study, we assessed the ability of six atypical ADs (clozapine, olanzapine, quetiapine, risperidone, aripiprazole, and ziprasidone) used in schizophrenia treatment to modulate oxidative damage to different biomolecules such as lipids and proteins. Patients and Methods We measured the levels of oxidative stress markers in plasma and urine: total antioxidant capacity by FRAP (according to a modified method of Benzie & Strain), thiobarbituric acid reactive species – TBARS (spectrophotometric method), 4-hydroxy-2-nonenal (4-HNE) (OxiSelect™ HNE Adduct Competitive ELISA Kit), 3-nitrotyrosine (3-NT) (OxiSelect™ Nitrotyrosine ELISA Kit) in plasma, and F2-isoprostanes (BIOXYTECH ® Urinary 8-epi-Prostaglandin F2α) in the urine of 60 schizophrenic patients (before and after treatment) and in 30 healthy subjects. Results Our results showed that in schizophrenic patients levels of lipid peroxidation markers (TBARS, F2-isoprostanes) were higher than in healthy subjects but FRAP in schizophrenic patients was lower than in healthy controls and increased after 4-week treatment with tested ADs. A 4-week treatment with ADs caused the improvement of psychopathology symptoms estimated by Positive and Negative Syndrome Scale (PANSS) that was accompanied by decreased lipid peroxidation (F2-isoprostanes, TBARS; p=2.9x10 −6 , p=7.6x10 −5 , respectively) and an increase in total antioxidative capacity (FRAP) (p=5.16x10 −16 ). Conclusion Atypical antipsychotics especially clozapine, olanzapine and quetiapine demonstrate the effective outcome of antipsychotic treatment, beneficial antioxidative action by reducing lipid peroxidation and increased total plasma antioxidant activity.

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Section: Discussionmentioning

confidence: 90%

Section: Discussionmentioning

confidence: 99%

Comparative Study of the Effects of Atypical Antipsychotic Drugs on Plasma and Urine Biomarkers of Oxidative Stress in Schizophrenic Patients

Dietrich‐Muszalska¹,

Kołodziejczyk-Czepas²,

Nowak³

2021

NDT

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Mechanisms of disordered neurodegenerative function: concepts and facts about the different roles of the protein kinase RNA-like endoplasmic reticulum kinase (PERK)

Taalab

Ibrahim

Maher³

et al. 2018

Reviews in the Neurosciences

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AbstractNeurodegenerative diseases, such as Alzheimer’s disease, Huntington’s disease, Parkinson’s disease, prion disease, and amyotrophic lateral sclerosis, are a dissimilar group of disorders that share a hallmark feature of accumulation of abnormal intraneuronal or extraneuronal misfolded/unfolded protein and are classified as protein misfolding disorders. Cellular and endoplasmic reticulum (ER) stress activates multiple signaling cascades of the unfolded protein response (UPR). Consequently, translational and transcriptional alterations in target gene expression occur in response directed toward restoring the ER capacity of proteostasis and reestablishing the cellular homeostasis. Evidences fromin vitroandin vivodisease models indicate that disruption of ER homeostasis causes abnormal protein aggregation that leads to synaptic and neuronal dysfunction. However, the exact mechanism by which it contributes to disease progression and pathophysiological changes remains vague. Downstream signaling pathways of UPR are fully integrated, yet with diverse unexpected outcomes in different disease models. Three well-identified ER stress sensors have been implicated in UPR, namely, inositol requiring enzyme 1, protein kinase RNA-activated-like ER kinase (PERK), and activating transcription factor 6. Although it cannot be denied that each of the involved stress sensor initiates a distinct downstream signaling pathway, it becomes increasingly clear that shared pathways are crucial in determining whether or not the UPR will guide the cells toward adaptive prosurvival or proapoptotic responses. We review a body of work on the mechanism of neurodegenerative diseases based on oxidative stress and cell death pathways with emphasis on the role of PERK.

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Platelet haemostatic function in psychiatric disorders: Effects of antidepressants and antipsychotic drugs

Dietrich‐Muszalska

Wachowicz

2016

The World Journal of Biological Psychiatry

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Objectives Platelets, the smallest anucleated blood cells, play an essential role in the first step of complex haemostatic process. This review presents the haemostatic function of blood platelets related to their activation in psychiatric disorders (schizophrenia, depression), the role of antipsychotic and antidepressant medication, and introduces the mechanisms by which activated platelets may be involved in the pathophysiology of these disorders. Methods Platelets are interesting and easily accessible blood cells to study biochemical pathways related to schizophrenia and other psychiatric disorders, and their complex activation process might be useful as a diagnostic peripheral marker for studying psychiatric disorders and haemostatic complications. Results The excessive activation of platelets observed in patients with depression and schizophrenia is involved in cardiovascular diseases, stroke and increased risk of thrombotic complications that may be major causes of morbidity and mortality of patients. The use of antidepressants or antipsychotic drugs in depression and schizophrenia treatment is often associated with haematological side effects such as bleeding, venous thromboembolism and impaired platelet function. Conclusions Understanding the role of platelet activation in psychiatric disorders such as schizophrenia or depression and medication may improve therapies in the future.

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The Role of Nitric Oxide and Nitrosative Stress in Schizophrenia

Cited by 3 publications

References 146 publications

Comparative Study of the Effects of Atypical Antipsychotic Drugs on Plasma and Urine Biomarkers of Oxidative Stress in Schizophrenic Patients

Comparative Study of the Effects of Atypical Antipsychotic Drugs on Plasma and Urine Biomarkers of Oxidative Stress in Schizophrenic Patients

Mechanisms of disordered neurodegenerative function: concepts and facts about the different roles of the protein kinase RNA-like endoplasmic reticulum kinase (PERK)

Platelet haemostatic function in psychiatric disorders: Effects of antidepressants and antipsychotic drugs

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