ArticleInternational journal of immunopathology and pharmacology2016
Role of oxidative stress in the pathophysiology of Toxoplasma gondii infection.
Article in International journal of immunopathology and pharmacology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.
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Who cites it
42 citing papers in PubMed, 63 citations in OpenAlex.
- Temporal Neuroimmune Changes During Primary and Persistent Experimental Toxoplasmic Encephalitis.International journal of molecular sciences · 2026Article
- Quercetin ReducesInternational journal of molecular sciences · 2026Article
- The Effect of Curcumin on Chronic Toxoplasma gondii Infection in the Testes of BALB/c Mice.Acta parasitologica · 2026Article
- ZBP1 mediated restriction of Toxoplasma gondii in both the early acute and chronic brain stages of infection.ImmunoHorizons · 2026Article
- Estudo Abrangente do Resveratrol Associado à Sulfadiazina em Linfócitos Infectados com Toxoplasma gondii: Envolvimento da Sinalização Purinérgica na Resposta Imunológica.Acta parasitologica · 2026Article
- Physical exercise protects against Toxoplasma gondii infection-induced muscle atrophy and microvascular rarefaction.Communications biology · 2026Article
- Study onPrevalence of Parasitic Infections Among Hepatitis C Virus Patients in Egypt.Archives of Razi Institute · 2025Article
- Cellular Senescence Contributes to Colonic Barrier Integrity Impairment Induced by Toxoplasma gondii Infection.Inflammation · 2025Article
- Contribution of the dopaminergic system in toxoplasmic encephalitis neuroimmunopathogenesis.Histology and histopathology · 2025Article
- Beyond Latency: ChronicBiomedicines · 2025Review
- Potential Correlation Between Molecular Biomarkers and Oxidative Stress in Traumatic Brain Injury.International journal of molecular sciences · 2025Review
- Anti-Antioxidants (Basel, Switzerland) · 2025Article
- Knockdown of DJ-1 Exacerbates Neuron Apoptosis Induced by TgCtwh3 through the NF-κB Pathway.Molecular neurobiology · 2025Article
- Anti-toxoplasma effect ofOpen veterinary journal · 2025Article
- First Description of the Role of the Relationship Between Serum Amyloid P Components and Nuclear Factors/Pro-Cytokines During Critical Periods of Toxoplasmic Encephalitis.Brain sciences · 2024Article
- Toxoplasma Gondii infection and cardiovascular mortality: sex-specific differences in a United States population-based cohort study.BMC infectious diseases · 2024Article
- Intestinal microbiota imbalance resulted by anti-Toxoplasma gondii immune responses aggravate gut and brain injury.Parasites & vectors · 2024Article
- Toxoplasma gondii infection associated with inflammasome activation and neuronal injury.Scientific reports · 2024Article
- ADAMTS-13 and HMGB1-induced oxidative stress in Taenia multiceps-infected animals.Scientific reports · 2023Article
- Metabolic changes to host cells withbioRxiv : the preprint server for biology · 2023Article
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Authors and funding
2 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Oxidative stress (OS) plays an essential role in the pathogenesis of common neurodegenerative diseases. We have previously shown that Toxoplasma gondii (T. gondii) induces high nitric oxide (NO) production, glial activation, and apoptosis that altogether cause severe neuropathology in toxoplasma encephalitis (TE). The objective of this study was to investigate the cytotoxic effect of OS and to identify a correlation between the causes of T. gondii induced neuropathology. Expression levels of glutathione reductase (GR), Cu/Zn superoxide dismutase (SOD1), neuron specific enolase (NSE), and 8-hydroxy-2'-deoxyguanosine (8-OHdG) were investigated. Results of the study revealed that the levels of GR (P <0.005) and NSE (P <0.001) expression in the brain tissue markedly increased while SOD1 activity decreased (P <0.001) in the infected group compared to the non-infected group. In addition, intense staining for 8-OHdG (P <0.05) was observed both in the nucleus and the cytoplasm of neurons and glial cells that underwent OS. These results were reasonable to suggest that T. gondii-mediated OS might play a pivotal role and a different type of role in the mechanism of neurodegeneration/neuropathology in the process of TE. The results also clearly indicated that increased levels of NO and apoptosis might contribute to OS-related pathogenesis of TE. As a result, OS and expression of NSE might give an idea of the disease progress and may have a critical diagnostic significance for patients with T. gondii infection.
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