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Partial Reversal of the in Vivo Antimalarial Activity of DDS against Plasmodium Berghei by Induced Hyperglycemia
Richard J. Cenedella
Richard J. Cenedella
Department of Pharmacology, West Virginia University Medical Center, Morgantown, West Virginia 26506
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L. H. Saxe
L. H. Saxe
Department of Pharmacology, West Virginia University Medical Center, Morgantown, West Virginia 26506
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Earlier observations, in vitro, demonstrated that the ability of 4,4′-diaminodiphenylsulfone (DDS) to inhibit the glucose utilization of intraerythrocytic Plasmodium berghei is antagonized by elevation of medium glucose levels. In this study we observed that a single oral dose of DDS (100 mg per kg) was less effective in depressing malaria infections in chronically hyperglycemic mice (blood-glucose levels of about 1,000 mg %) than in normoglycemic mice. Unparasitized normoglycemic and diabetic mice possess similar whole-blood DDS levels during the 24 hr after oral dosage with 100 mg per kg of DDS. After treatment of normoglycemic, P. berghei-infected rats with a single oral dose of DDS (100 mg per kg), the parasitized blood cells removed from these animals 6 hours later consumed less glucose than identically parasitized cells from untreated rats. These observations support the possibility that DDS exerts a portion of its antimalarial activity in vivo through inhibition of utilization of intraerythrocytic parasite glucose.
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