ArticleIranian journal of pharmaceutical research : IJPR2014
Schizophrenia induces oxidative stress and cytochrome C release in isolated rat brain mitochondria: a possible pathway for induction of apoptosis and neurodegeneration.
Article in Iranian journal of pharmaceutical research : IJPR, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
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Who cites it
31 citing papers in PubMed, 56 citations in OpenAlex.
- Investigating the effects of chlorogenic acid on novel object recognition memory impairment, hyperlocomotion, and prefrontal BDNF expression in a sub-chronic ketamine-induced schizophrenia-like rat model.IBRO neuroscience reports · 2026Article
- Mitochondria-mediated anticancer effects of two previously characterized COX-2 inhibitors in hepatocellular carcinoma.Molecular and cellular biochemistry · 2026Article
- Cerebrolysin ameliorates ketamine-mediated anxiety and cognitive impairments via modulation of mitochondrial function and CREB/PGC-1α pathway.Molecular brain · 2025Article
- Ketamine and olanzapine alter behaviour and prefrontal-cortex BDNF differentially in male and female rats.Scientific reports · 2025Article
- Ancestral retrovirus envelope protein ERVWE1 upregulates circ_0001810, a potential biomarker for schizophrenia, and induces neuronal mitochondrial dysfunction via activating AK2.Cell & bioscience · 2024Article
- Capsaicin alleviates neuronal apoptosis and schizophrenia-like behavioral abnormalities induced by early life stress.Schizophrenia (Heidelberg, Germany) · 2023Article
- L-Carnitine Prevents Behavioural Alterations in Ketamine-Induced Schizophrenia in Mice: Possible Involvement of Oxidative Stress and Inflammation Pathways.Journal of toxicology · 2023Article
- Systematic Review of the Therapeutic Role of Apoptotic Inhibitors in Neurodegeneration and Their Potential Use in Schizophrenia.Antioxidants (Basel, Switzerland) · 2022Review
- Review
- Recent Reports on Redox Stress-Induced Mitochondrial DNA Variations, Neuroglial Interactions, and NMDA Receptor System in Pathophysiology of Schizophrenia.Molecular neurobiology · 2022Review
- Do Autophagy Enhancers/ROS Scavengers Alleviate Consequences of Mild Mitochondrial Dysfunction Induced in Neuronal-Derived Cells?International journal of molecular sciences · 2021Article
- Protective Effect of Crocin against Mitochondrial Damage and Memory Deficit Induced by Beta-amyloid in the Hippocampus of Rats.Iranian journal of pharmaceutical research : IJPR · 2021Article
- Oxidative Stress and the Pathophysiology and Symptom Profile of Schizophrenia Spectrum Disorders.Frontiers in psychiatry · 2021Review
- Article
- Energization by multiple substrates and calcium challenge reveal dysfunctions in brain mitochondria in a model related to acute psychosis.Journal of bioenergetics and biomembranes · 2020Article
- Clozapine protects adult neural stem cells from ketamine-induced cell death in correlation with decreased apoptosis and autophagy.Bioscience reports · 2020Article
- Mitochondrial Dysfunction and Changes in High-Energy Compounds in Different Cellular Models Associated to Hypoxia: Implication to Schizophrenia.Scientific reports · 2019Article
- A Review on Toxicodynamics of Depleted Uranium.Iranian journal of pharmaceutical research : IJPR · 2019Review
- Methylmercury exposure develops atherosclerotic risk factors in the aorta and programmed cell death in the cerebellum: ameliorative action of Celastrus paniculatus ethanolic extract in male Wistar rats.Environmental science and pollution research international · 2018Article
- Protein-Protein Interaction Analysis of Common Top Genes in Obsessive-Compulsive Disorder (OCD) and Schizophrenia: Towards New Drug Approach Obsessive-Compulsive disorder (OCD) and Schizophrenia Comorbidity Gene Analysis.Iranian journal of pharmaceutical research : IJPR · 2018Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Schizophrenia is a chronic and often debilitating illness which affects about 1% of the world population. Some reagents have been used to simulate schizophrenic disorders in laboratory animals, such as amphetamine and ketamine. Previous studies have suggested that reactive oxygen species (ROS) production, reduced levels of ATP, mitochondrial dysfunction and apoptosis are involved in the pathophysiology and etiology of schizophrenia. In this study we divided Wistar rats in to 2 groups; control group received normal saline and test group received ketamine 30 mg/Kg daily for five consecutive days. Then, locomotor activity including side to side head rocking and arcing of neck, proved schizophrenia in the test group rats. Rats in both control and test groups were then decapitated and brain mitochondria were isolated. Our results showed increased ROS formation, mitochondrial membrane potential collapse, mitochondrial swelling and cytochrome c release in mitochondria of schizophrenic test group. Our findings suggested that mitochondrial ROS formation and apoptosis signaling are likely involved in cellular pathology of Schizophrenia. To our knowledge this is the first report that provides a mechanistic justification between mitochondrial events and neuodegeneration in the Schizophrenia.
Indexed as
Identifiers
24711834PMC3977058W1488150120What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.