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Molecular Pharmacology, Vol 4, 407-410, Copyright © 1968 by the American Society for Pharmacology and Experimental Therapeutics
1 Department of Pathobiology, The Johns Hopkins University School of Hygiene and
Public Health, Baltimore, Maryland 2l205
Several anticestodal drugs were shown previously to inhibit the mitochondrial 32P-ATP exchange reaction in the cestode Hymenolepis diminuta. It was postulated, on the basis of similarities in their energy metabolism, that the same anticestodal agents should also inhibit the exchange reaction in the mitochondria of the nematode, Ascaris lumbricoides. Most of these compounds did effectively inhibit the reaction in the nematode mitochondria, indicating that the selective toxicity for cestodes is a result of differences in permeability between the two groups of helminths.
Note:
ACKNOWLEDGMENTS
This investigation was supported in part by
Grants AI 05290 and 5T01-AI-00149 from the
National Institutes of Health, United States
Public Health Service.
We would like to thank Drs. L. Runeberg,
O. D. Standen, K. Bowden, R. Gönnert, and J. L.
Morrison for supplying anticestodal drugs and the
5-nitrofurfurylidine hydrazide of 3,5-dinitrosalicylic
acid. We also wish to thank the Schluderberg-Kurdle Company, Inc. (Baltimore), for its
generous help in the collection of the adult
ascarids used in these investigations.