@article{oai:obihiro.repo.nii.ac.jp:00004336,
 author = {Suzuki, Hiroshi and Kume, Aiko and Herbas, Marua Shirely},
 issue = {1},
 journal = {International Journal of Molecular Sciences},
 month = {},
 note = {application/pdf, Although epidemiological and experimental studies have suggested beneficial effects of vitamin E deficiency on malaria infection, it has not been clinically applicable for the treatment of malaria owing to the significant content of vitamin E in our daily food. However, since α-tocopherol transfer protein (α-TTP) has been shown to be a determinant of vitamin E level in circulation, manipulation of α-tocopherol levels by α-TTP inhibition was considered as a potential therapeutic strategy for malaria. Knockout studies in mice indicated that inhibition of α-TTP confers resistance against malaria infections in murines, accompanied by oxidative stress-induced DNA damage in the parasite, arising from vitamin E deficiency. Combination therapy with chloroquine and α-TTP inhibition significantly improved the survival rates in murines with malaria. Thus, clinical application of α-tocopherol deficiency could be possible, provided that α-tocopherol concentration in circulation is reduced. Probucol, a recently found drug, induced α-tocopherol deficiency in circulation and was effective against murine malaria. Currently, treatment of malaria relies on the artemisinin-based combination therapy (ACT); however, when mice infected with malarial parasites were treated with probucol and dihydroartemisinin, the beneficial effect of ACT was pronounced. Protective effects of vitamin E deficiency might be extended to manage other parasites in future. © 2018 by the authors. Licensee MDPI, Basel, Switzerland.},
 title = {Potential of vitamin E deficiency, induced by inhibition of α-tocopherol efflux, in murine malaria infection},
 volume = {20},
 year = {2019}
}