ArticlePloS one2015
Probucol-Induced α-Tocopherol Deficiency Protects Mice against Malaria Infection.
Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 15 citations in OpenAlex.
- Probucol mitigates high-fat diet-induced cognitive and social impairments by regulating brain redox and insulin resistance.Frontiers in neuroscience · 2024Article
- Micromolar Dihydroartemisinin Concentrations Elicit Lipoperoxidation inAntioxidants (Basel, Switzerland) · 2023Article
- Application of regulation of reactive oxygen species and lipid peroxidation to disease treatment.Journal of clinical biochemistry and nutrition · 2023Article
- Effect of α-Tocopheryloxy Acetic Acid on the Infection of Mice with Plasmodium berghei ANKA In Vivo and Humans with P. falciparum In Vitro.Acta parasitologica · 2022Article
- Probucol induces the generation of lipid peroxidation products in erythrocytes and plasma of male cynomolgus macaques.Journal of clinical biochemistry and nutrition · 2019Article
- Potential of Vitamin E Deficiency, Induced by Inhibition of α-Tocopherol Efflux, in Murine Malaria Infection.International journal of molecular sciences · 2018Review
- α-Tocopheryl succinate-suppressed development of cerebral malaria in mice.Parasitology research · 2018Article
- Host genetics in malaria: lessons from mouse studies.Mammalian genome : official journal of the International Mammalian Genome Society · 2018Review
- Probucol dramatically enhances dihydroartemisinin effect in murine malaria.Malaria journal · 2016Article
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The emergence of malaria pathogens having resistance against antimalarials implies the necessity for the development of new drugs. Recently, we have demonstrated a resistance against malaria infection of α-tocopherol transfer protein knockout mice showing undetectable plasma levels of α-tocopherol, a lipid-soluble antioxidant. However, dietary restriction induced α-tocopherol deficiency is difficult to be applied as a clinical antimalarial therapy. Here, we report on a new strategy to potentially treat malaria by using probucol, a drug that can reduce the plasma α-tocopherol concentration. Probucol pre-treatment for 2 weeks and treatment throughout the infection rescued from death of mice infected with Plasmodium yoelii XL-17 or P. berghei ANKA. In addition, survival was extended when the treatment started immediately after parasite inoculation. The ratio of lipid peroxidation products to parent lipids increased in plasma after 2 weeks treatment of probucol. This indicates that the protective effect of probucol might be mediated by the oxidative stressful environment induced by α-tocopherol deficiency. Probucol in combination with dihydroartemisin suppressed the proliferation of P. yoelii XL-17. These results indicated that probucol might be a candidate for a drug against malaria infection by inducing α-tocopherol deficiency without dietary α-tocopherol restriction.
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