Hypoxanthine transport in the insect trypanosome, Crithidia luciliae,
was activated in purine depleted conditions. The existence of 2 hypoxa
nthine transport mechanisms was established. The first, a non-saturabl
e diffusion system, present in purine replete conditions, exhibited pr
operties that were different from the second transport system which wa
s evident only during purine depleted conditions (purine stress). The
rate of transport under purine stress was elevated approximately 8-fol
d over that in replete conditions. This transporter was saturable with
a K-m of 3 . 9 mu M for hypoxanthine. The transporter substrate speci
ficity included other purine bases, e.g. adenine and guanine, and the
purine nucleoside, adenosine. These inhibited hypoxanthine transport c
ompetitively with K-i values of 2 mu M, 3 mu M and 42 mu M respectivel
y. Coincident with the increase of hypoxanthine transport under purine
stress, the transport of adenosine increased 4-fold and the activity
of the 3'-nucleotidase ectoenzyme also increased significantly. Under
purine stress the concurrent increase of hypoxanthine and adenosine tr
ansport and the increase in 3'-nucleotidase activity could be represse
d with either the supplementation of excess purines or by cycloheximid
e. This study of purine salvage mechanisms in Crithidia luciliae illus
trates the successful adaptation of the parasite to nutritional insuff
iciency.