The testis is the third common site of relapse in childhood acute lymp
hoblastic leukemia (ALL). Despite the apparent clinical importance of
testicular relapse, its pathogenesis is still unknown. The studies wit
h an animal model of ALL have shown that many testicular factors are a
ble to control the intratesticular infiltration and proliferation of l
eukemic lymphoblasts during the untreated course of ALL. In the presen
t study, the ultrastructure of rat testicular interstitium infiltrated
by leukemic lymphoblasts was studied in two groups of rats transplant
ed with rat T cell leukemia in early and late puberty. In both groups
most of the leukemic cells infiltrating testicular interstitium were t
otally or partly enveloped by one or more Leydig cells, and the endoth
elial cells of capillaries, arterioles and venules were hypertrophic.
The Leydig cells of the younger experimental group were by nuclear and
cytoplasmic ultrastructure similar to the undifferentiated Leydig cel
ls normally seen on the third postnatal week. The results suggest that
Leydig cells bind leukemic lymphoblasts on their surface in vivo as a
lso previously observed in vitro, and that ALL may disturb the puberta
l maturation of Leydig cells. The occlusion of arterial and capillary
lumina by folds of hypertrophic endothelial cells together with adhere
d leukemic lymphoblasts may impair the circulation of leukemic testes.