ArticlePloS one2013
Investigation of hydrogen sulfide gas as a treatment against P. falciparum, murine cerebral malaria, and the importance of thiolation state in the development of cerebral malaria.
Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
8 citing papers in PubMed, 12 citations in OpenAlex.
- The Role of Biofilm-Derived Compounds in Microbial and Protozoan Interactions.Microorganisms · 2025Review
- Impact of Reactive Sulfur Species onAntioxidants (Basel, Switzerland) · 2024Article
- Genetics of cerebral malaria: pathogenesis, biomarkers and emerging therapeutic interventions.Cell & bioscience · 2022Review
- Hydrogen sulfide protects against the development of experimental cerebral malaria in a C57BL/6 mouse model.Molecular medicine reports · 2017Article
- Glucagon-like peptide-1 analogue, liraglutide, in experimental cerebral malaria: implications for the role of oxidative stress in cerebral malaria.Malaria journal · 2016Article
- Pathophysiological Mechanisms in Gaseous Therapies for Severe Malaria.Infection and immunity · 2016Review
- Pathogenesis of cerebral malaria: new diagnostic tools, biomarkers, and therapeutic approaches.Frontiers in cellular and infection microbiology · 2015Review
- Systemic and Cerebral Vascular Endothelial Growth Factor Levels Increase in Murine Cerebral Malaria along with Increased Calpain and Caspase Activity and Can be Reduced by Erythropoietin Treatment.Frontiers in immunology · 2014Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
introductionCerebral malaria (CM) is a potentially fatal cerebrovascular disease of complex pathogenesis caused by Plasmodium falciparum. Hydrogen sulfide (HS) is a physiological gas, similar to nitric oxide and carbon monoxide, involved in cellular metabolism, vascular tension, inflammation, and cell death. HS treatment has shown promising results as a therapy for cardio- and neuro- pathology. This study investigates the effects of fast (NaHS) and slow (GYY4137) HS-releasing drugs on the growth and metabolism of P. falciparum and the development of P. berghei ANKA CM. Moreover, we investigate the role of free plasma thiols and cell surface thiols in the pathogenesis of CM.
methodsP. falciparum was cultured in vitro with varying doses of HS releasing drugs compared with artesunate. Growth and metabolism were quantified. C57Bl/6 mice were infected with P. berghei ANKA and were treated with varying doses and regimes of HS-releasing drugs. Free plasma thiols and cell surface thiols were quantified in CM mice and age-matched healthy controls.
resultsHS-releasing drugs significantly and dose-dependently inhibited P. falciparum growth and metabolism. Treatment of CM did not affect P. berghei growth, or development of CM. Interestingly, CM was associated with lower free plasma thiols, reduced leukocyte+erythrocyte cell surface thiols (infection day 3), and markedly (5-fold) increased platelet cell surface thiols (infection day 7).
conclusionsHS inhibits P. falciparum growth and metabolism in vitro. Reduction in free plasma thiols, cell surface thiols and a marked increase in platelet cell surface thiols are associated with development of CM. HS drugs were not effective in vivo against murine CM.
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