@article{oai:obihiro.repo.nii.ac.jp:00004376,
 author = {Shichiri, Mototada and Ishida, Noriko and Hagihara, Yoshihisa and Yoshida, Yasukazu and Kume, Aiko and Suzuki, Hiroshi},
 issue = {2},
 journal = {Journal of Clinical Biochemistry and Nutrition},
 month = {Mar},
 note = {application/pdf, We previously reported that probucol, a lipid lowering agent, protected mice from malaria infection via depletion in plasma α tocopherol. The antioxidant αtocopherol in host circulation is necessary for the malaria parasites to protect themselves from oxidative stress in erythrocytes where high amounts of reactive oxygen species are generated. To assess the potential for the clinical application of probucol as an antimalarial therapy, it was necessary to determine the effects of probucol by using primate experiments. Here we verified that probucol induces an α tocopherol decrement in cynomolgus macaque erythrocytes and plasma. After 2 weeks of probucol administration at doses of 200 or 400 mg/kg/day, the αtocopherol contents in erythrocytes tended to decrease. The contents of hydroxyoctadecadienoic acids and 7βhydroxycholesterol, peroxidation products derived from linoleic acid and cholesterol, respectively, increased in erythrocytes. On the other hand, plasma αtocopherol concentration showed a marginal decrement. Plasma lipid peroxidation products were transiently increased in the early stages of probucol administration. No adverse effects were observed throughout the experiment, although the dosage of probucol was higher than the clinical maximum dosage. Considering that malaria proliferates in erythrocytes, probucolinduced disruption of redox homeostasis in erythrocytes could be effective in the inhibition of parasite proliferation. © 2019 JCBN.},
 pages = {129--142},
 title = {Probucol induces the generation of lipid peroxidation products in erythrocytes and plasma of male cynomolgus macaques},
 volume = {64},
 year = {2019}
}