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10.1371/journal.pone.0136014 http://scihub22266oqcxt.onion/10.1371/journal.pone.0136014 26296197!4546625!26296197     free     free     free Deprecated: Implicit conversion from float 229.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 229.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 229.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 229.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 229.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       PLoS+One 2015 ; 10 (8): e0136014 Nephropedia Template TP {{tp|p=26296197|t=2015. Probucol-Induced alpha-Tocopherol Deficiency Protects Mice against Malaria Infection |pdf=|usr=}}{{26296197}} gab.com Text Probucol-Induced alpha-Tocopherol Deficiency Protects Mice against Malaria Infection JO: PLoS One http://www.kidney.de/pget.php?&tw=1&pmid=26296197 #FOAvip 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 alpha-tocopherol transfer protein knockout mice showing undetectable plasma levels of alpha-tocopherol, a lipid-soluble antioxidant. However, dietary restriction induced alpha-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 alpha-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 alpha-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 alpha-tocopherol deficiency without dietary alpha-tocopherol restriction. Twit Text FOAVip Probucol-Induced alpha-Tocopherol Deficiency Protects Mice against Malaria Infection ????PLoS One http://www.kidney.de/pget.php?&tw=1&pmid=26296197 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26296197 #FOAvip English Wikipedia <ref>{{Cite pmid|26296197}}</ref> Probucol-Induced alpha-Tocopherol Deficiency Protects Mice against Malaria Infection #MMPMID26296197 Herbas MS; Shichiri M; Ishida N; Kume A; Hagihara Y; Yoshida Y; Suzuki H PLoS One 2015[]; 10 (8): e0136014 PMID26296197show ga 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 alpha-tocopherol transfer protein knockout mice showing undetectable plasma levels of alpha-tocopherol, a lipid-soluble antioxidant. However, dietary restriction induced alpha-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 alpha-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 alpha-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 alpha-tocopherol deficiency without dietary alpha-tocopherol restriction. |Animals[MESH] |Antimalarials/*pharmacology[MESH] |Antioxidants/metabolism/*pharmacology[MESH] |Artemisinins/*pharmacology[MESH] |Drug Administration Schedule[MESH] |Drug Synergism[MESH] |Drug Therapy, Combination[MESH] |Female[MESH] |Lipid Peroxidation/drug effects[MESH] |Malaria/blood/*drug therapy/parasitology/pathology[MESH] |Male[MESH] |Mice[MESH] |Mice, Inbred C57BL[MESH] |Oxidative Stress[MESH] |Parasitemia/blood/*drug therapy/pathology[MESH] |Plasmodium berghei/drug effects/physiology[MESH] |Plasmodium yoelii/drug effects/physiology[MESH] |Probucol/*pharmacology[MESH] |Survival Analysis[MESH]Probucol-Induced alpha-Tocopherol Deficiency Protects Mice against Mal(epmc).pdf DeepDyve Pubget Overpricing