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Specificity of the Glucose Transport System in Leishmania tropica Promastigotes *
Author(s) -
SCHAEFER FRANK W.,
MUKKADA ANTONY J.
Publication year - 1976
Publication title -
the journal of protozoology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.067
H-Index - 77
eISSN - 1550-7408
pISSN - 0022-3921
DOI - 10.1111/j.1550-7408.1976.tb03810.x
Subject(s) - leishmania tropica , leishmania , microbiology and biotechnology , biology , chemistry , leishmaniasis , parasite hosting , cutaneous leishmaniasis , immunology , computer science , world wide web
SYNOPSIS. The glucose transport system in Leishmania tropica promastigotes was characterized by the use of labeled 2‐deoxy‐D‐glucose (2‐DOG), a nonmetabolizable glucose analog. The uptake system has a Q 10 of 2 and a heat of activation of 10.2 kcal/mole. The glucose transport system is subject to competitive inhibition by 2‐DOG, glucosamine, N ‐acetyl glucosamine, mannose, galactose, and fructose which suggests that substitutions in the hexose chain at carbons 2 and 4 do not affect carrier specificity. In contrast, changes at carbon 1 (α‐methyl‐D‐glucoside, 1,5‐anhydroglucitol) and carbon 3 (3–0‐methyl glucose) lead to loss of carrier affinity since these sugars do not compete for the glucose carrier. Sugars that compete with the glucose carrier have one common feature—they all exist in the pyranose form in solution. The carrier for D‐glucose does not interact with L‐glucose or any of the pentose sugars tested. Uptake of 2‐DOG is inhibited by glycerol. This inhibition, however, is noncompetitive; it is evident, therefore, that glucose and glycerol do not compete for the same carrier. Glycerol does not repress the glucose carrier since cells grown in presence of glycerol transport the sugar normally.