ArticleJournal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology2012
S-nitrosoglutathione prevents experimental cerebral malaria.
Article in Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 29 citations in OpenAlex.
- Selenite Interacting with Thiols Catalytically Releases NO from GSNO, Cleaves Plasmid DNA and Reduces the Hypotensive Effect of GSNO in Rats.Biological trace element research · 2026Article
- Determinants of retinopathy and short-term neurological outcomes after cerebral malaria.Scientific reports · 2025Article
- Elevated plasma interleukin-8 as a risk factor for mortality in children presenting with cerebral malaria.Infectious diseases of poverty · 2023Article
- Roles and current applications of S-nitrosoglutathione in anti-infective biomaterials.Materials today. Bio · 2022Review
- S-nitrosoglutathione reductase (GSNOR) inhibitor as an immune modulator in experimental autoimmune encephalomyelitis.Free radical biology & medicine · 2018Article
- Article
- Hypoxia inducible factor-1 alpha stabilization for regenerative therapy in traumatic brain injury.Neural regeneration research · 2017Review
- Perforin Expression by CD8 T Cells Is Sufficient To Cause Fatal Brain Edema during Experimental Cerebral Malaria.Infection and immunity · 2017Article
- Pathophysiological Mechanisms in Gaseous Therapies for Severe Malaria.Infection and immunity · 2016Review
- NO-Donor Dihydroartemisinin Derivatives as Multitarget Agents for the Treatment of Cerebral Malaria.Journal of medicinal chemistry · 2015Article
- Article
- Experimental cerebral malaria pathogenesis--hemodynamics at the blood brain barrier.PLoS pathogens · 2014Article
- Vascular dysfunction as a target for adjuvant therapy in cerebral malaria.Memorias do Instituto Oswaldo Cruz · 2014Review
- Potential efficacy of citicoline as adjunct therapy in treatment of cerebral malaria.Antimicrobial agents and chemotherapy · 2014Article
- Transdermal glyceryl trinitrate as an effective adjunctive treatment with artemether for late-stage experimental cerebral malaria.Antimicrobial agents and chemotherapy · 2013Article
- A new hypothesis on the manifestation of cerebral malaria: the secret is in the liver.Medical hypotheses · 2013Article
- Article
- Nitric oxide synthase dysfunction contributes to impaired cerebroarteriolar reactivity in experimental cerebral malaria.PLoS pathogens · 2013Article
- The inhibitory effect of S-nitrosoglutathione on blood-brain barrier disruption and peroxynitrite formation in a rat model of experimental stroke.Journal of neurochemistry · 2012Article
- An NO/GSNO-based Neuroregeneration Strategy for Stroke Therapy.Journal of neurology and neuroscienceArticle
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Authors and funding
5 authors at 3 institutions in 2 countries.
Funding
Abstract
Administration of the exogenous nitric oxide (NO) donor dipropylenetriamine-NONOate (DPTA-NO) to mice during Plasmodium berghei ANKA (PbA) infection largely prevents development of experimental cerebral malaria (ECM). However, a high dose (1 mg/mouse twice a day) is necessary and causes potent side effects such as marked hypotension. In the present study we evaluated whether an alternative, physiologically relevant NO donor, S-nitrosoglutathione (GSNO), was able to prevent ECM at lower doses with minimal side effects. Prophylactic treatment with high (3.5 mg), intermediate (0.35 mg) or low (0.035 mg) doses of GSNO decreased incidence of ECM in PbA-infected mice, decreasing also edema, leukocyte accumulation and hemorrhage incidence in the brain. The high dose inhibited parasite growth and also induced transient hypotension. Low and intermediate doses had no or only mild effects on parasitemia, blood pressure, and heart rate compared to saline-treated mice. PbA infection decreased brain total and reduced (GSH) glutathione levels. Brain levels of oxidized (GSSG) glutathione and the GSH/GSSG ratio were positively correlated with temperature and motor behavior. Low and intermediate doses of GSNO failed to restore the depleted brain total glutathione and GSH levels, suggesting that ECM prevention by GSNO was probably related to other effects such as inhibition of inflammation and vascular protection. These results indicate that ECM is associated with depletion of the brain glutathione pool and that GSNO is able to prevent ECM development in a wide range of doses, decreasing brain inflammation and inducing milder cardiovascular side effects.
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