Glucose-6-phosphate dehydrogenase and catalase activities in erythrocytes of schizophrenic patients under pharmacotherapy with traditional antipsychotics

Ivanova, Svetlana A.; Smirnova, L.; Shchigoreva, Yu. G.; Boiko, Anastasiia S.; Semke, A.; Узбеков, М. Г.; Бохан, Н. А.

doi:10.1134/s1819712414010061

Cited by 13 publications

(6 citation statements)

References 13 publications

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“…Nevertheless, even after the treatment, the activity of MAO was significantly high er than in the control group, indicating that the therapy failed to normalize the MAO activity and metabolism as a whole [79]. In line with these observations, Ivanova et al [80] reported that the antipsychotic treatment of patients with chronic schizophrenia noticeably improved the clin ical signs, but the metabolic processes, e.g., those involv ing glucose 6 phosphate dehydrogenase (one of most important enzymes), remained significantly disrupted.…”

Section: Mental Disordersmentioning

confidence: 71%

Monoamine Oxidase as a Potential Biomarker of the Efficacy of Treatment of Mental Disorders

Узбеков

2021

Biochemistry Moscow

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The review summarizes the results of our own studies and published data on the biological markers of psychiatric disorders, with special emphasis on the activity of platelet monoamine oxidase. Pharmacotherapy studies in patients with the mixed anxiety-depressive disorder and first episode of schizophrenia have shown that the activity of platelet monoamine oxidase could serve as a potential biomarker of the efficacy of therapeutic interventions in these diseases.

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Section: Mental Disordersmentioning

confidence: 71%

Monoamine Oxidase as a Potential Biomarker of the Efficacy of Treatment of Mental Disorders

Узбеков

2021

Biochemistry Moscow

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“…In this study, we showed that FGA did not significantly change the GPx activity, while both FGA and SGA significantly decreased the catalase activity. The lowest catalase activity was found in patients treated with both type of medicaments, despite the evidence showing that therapy with FGA antipsychotics leads to the normalization of catalase activity [ 55 ]. These results indicate more pronounced oxidative stress in patients who received both types of antipsychotics.…”

Section: Discussionmentioning

confidence: 99%

Decreased Activity of Erythrocyte Catalase and Glutathione Peroxidase in Patients with Schizophrenia

et al. 2022

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Background and Objectives: Catalase and glutathione peroxidase (GPx) are important antioxidant enzymes that break down hydrogen peroxide (H2O2) in order to control its intracellular concentration, thus enabling its physiological role and preventing toxic effects. A lack or disruption of their function leads to the accumulation of hydrogen peroxide and the occurrence of oxidative stress. Accumulating studies have shown that the activities of key antioxidant enzymes are impaired in patients with schizophrenia. Since the published results are contradictory, and our previous studies found significantly higher erythrocyte superoxide dismutase (SOD) activity in patients with schizophrenia, the aim of this study was to determine the activity of enzymes that degrade hydrogen peroxide in the same group of patients, as well as to examine their dependence on clinical symptoms, therapy, and parameters associated with this disease. Materials and Methods: Catalase and GPx activities were determined in the erythrocytes of 68 inpatients with schizophrenia and 59 age- and gender-matched healthy controls. The clinical assessment of patients was performed by using the Positive and Negative Syndrome Scale (PANSS). The catalase activity was measured by the kinetic spectrophotometric method, while the GPx activity was determined by the commercially available Ransel test. Results: Erythrocyte catalase and GPx activities were significantly lower (p < 0.001 and p < 0.01, respectively) in subjects with schizophrenia than they were in healthy individuals. Lower catalase activity does not depend on heredity, disease onset, the number of episodes, or disease duration, while GPx activity showed significant changes in patients who had more than one episode and in those who had been suffering from the disease for over a year. Significantly lower catalase activity was noted in the PANSS(+/−) group in comparison with the PANSS(+) and PANSS(−) groups. The lowest catalase activity was found in subjects who were simultaneously treated with first- and second-generation antipsychotics; this was significantly lower than it was in those who received only one class of antipsychotics. Conclusion: These results indicate the presence of oxidative stress in the first years of clinically manifested schizophrenia and its dependence on the number of psychotic episodes, illness duration, predominant symptomatology, and antipsychotic medication.

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“…In our work, it was shown that therapy with typical antipsychotics leads to normalization of catalase activity. However, the activity of glucose-6-phosphate dehydrogenase continues to decrease [ 360 ]. Besides, we showed that antipsychotic therapy leads to a decrease in MDA in red blood cells and blood plasma but does not affect the level of oxidized and reduced glutathione [ 361 ].…”

Section: Antipsychotic Medication and Redox Correction In Schizophmentioning

confidence: 99%

Oxidative Stress‐Related Mechanisms in Schizophrenia Pathogenesis and New Treatment Perspectives

Ermakov

Dmitrieva

Parshukova

et al. 2021

Oxidative Medicine and Cellular Longevity

125

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Schizophrenia is recognized to be a highly heterogeneous disease at various levels, from genetics to clinical manifestations and treatment sensitivity. This heterogeneity is also reflected in the variety of oxidative stress-related mechanisms contributing to the phenotypic realization and manifestation of schizophrenia. At the molecular level, these mechanisms are supposed to include genetic causes that increase the susceptibility of individuals to oxidative stress and lead to gene expression dysregulation caused by abnormal regulation of redox-sensitive transcriptional factors, noncoding RNAs, and epigenetic mechanisms favored by environmental insults. These changes form the basis of the prooxidant state and lead to altered redox signaling related to glutathione deficiency and impaired expression and function of redox-sensitive transcriptional factors (Nrf2, NF-κB, FoxO, etc.). At the cellular level, these changes lead to mitochondrial dysfunction and metabolic abnormalities that contribute to aberrant neuronal development, abnormal myelination, neurotransmitter anomalies, and dysfunction of parvalbumin-positive interneurons. Immune dysfunction also contributes to redox imbalance. At the whole-organism level, all these mechanisms ultimately contribute to the manifestation and development of schizophrenia. In this review, we consider oxidative stress-related mechanisms and new treatment perspectives associated with the correction of redox imbalance in schizophrenia. We suggest that not only antioxidants but also redox-regulated transcription factor-targeting drugs (including Nrf2 and FoxO activators or NF-κB inhibitors) have great promise in schizophrenia. But it is necessary to develop the stratification criteria of schizophrenia patients based on oxidative stress-related markers for the administration of redox-correcting treatment.

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Glucose-6-phosphate dehydrogenase and catalase activities in erythrocytes of schizophrenic patients under pharmacotherapy with traditional antipsychotics

Cited by 13 publications

References 13 publications

Monoamine Oxidase as a Potential Biomarker of the Efficacy of Treatment of Mental Disorders

Monoamine Oxidase as a Potential Biomarker of the Efficacy of Treatment of Mental Disorders

Decreased Activity of Erythrocyte Catalase and Glutathione Peroxidase in Patients with Schizophrenia

Oxidative Stress‐Related Mechanisms in Schizophrenia Pathogenesis and New Treatment Perspectives

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