Reactions of Leydig cells and blood vessels to lymphoblastic leukemia in the rat testis.
The testis is the third common site of relapse in childhood acute lymphoblastic leukemia (ALL). Despite the apparent clinical importance of testicular relapse, its pathogenesis is still unknown. The studies with an animal model of ALL have shown that many testicular factors are able to control the intratesticular infiltration and proliferation of leukemic lymphoblasts during the untreated course of ALL. In the present study, the ultrastructure of rat testicular interstitium infiltrated by leukemic lymphoblasts was studied in two groups of rats transplanted with rat T cell leukemia in early and late puberty. In both groups most of the leukemic cells infiltrating testicular interstitium were totally or partly enveloped by one or more Leydig cells, and the endothelial 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 cells normally seen on the third postnatal week. The results suggest that Leydig cells bind leukemic lymphoblasts on their surface in vivo as also previously observed in vitro, and that ALL may disturb the pubertal maturation of Leydig cells. The occlusion of arterial and capillary lumina by folds of hypertrophic endothelial cells together with adhered leukemic lymphoblasts may impair the circulation of leukemic testes.
Jahnukainen
K
K
Department of Anatomy, University of Turku, Finland.
Saari
T
T
Salmi
T T
TT
Pöllänen
P
P
Pelliniemi
L J
LJ
D000818:Animals; D001808:Blood Vessels / Q000473:pathology; D003593:Cytoplasm / Q000648:ultrastructure; D004195:Disease Models, Animal; D017254:Leukemic Infiltration; D007985:Leydig Cells / Q000473:pathology* / Q000648:ultrastructure; D008297:Male; D008854:Microscopy, Electron; D009368:Neoplasm Transplantation; D054198:Precursor Cell Lymphoblastic Leukemia-Lymphoma / Q000473:pathology*; D051381:Rats; D013737:Testis / Q000098:blood supply* / Q000473:pathology* / Q000648:ultrastructure