Inhibition of Testicular Testosterone Biosynthesis Following Experimental Varicocele in Rats

In an attempt to determine whether defective testicular testosterone (T) biosynthesis may be associated with a varicocele, an experimental study was performed in adult rats whereby a unilateral left varicocele was surgically created. At 2, 4, 8, and 12 wk following the creation of the varicocele, intratesticular T as well as the activities of three (17α-hydroxylase, 17,20-desmolase, and 17β-hydroxysteroid dehydrogenase) of the five enzymes in the Δ4 pathway of testicular T biosynthesis were measured. Intratesticular T (ng/g testis ± SEM) in the left testis decreased significantly from 121 ± 21 in the control group to 59 ± 8 in the two-wk varicocele group (p < 0.01), and remained significantly suppressed throughout the experimental period. The T concentrations in the right testis paralleled those in the left in both the control and varicocele animals. At 2 wk following the creation of the varicocele, the activity (nmol/min/testis ± SEM) of the 17,20-desmolase enzyme decreased significantly, from 115 ± 8 in the left testis of control rats to 87 ± 6 in the left testis of the varicocele animals (p < 0.025), and remained low throughout the 12 weeks of the study. The activity of the 17α-hydroxylase enzyme was significantly decreased at the 8th and 12th weeks of the study, while the 17β-hydroxysteroid dehydrogenase activity did not show any significant change during the study period. The enzyme activities in the right testis paralleled those in the left testis. These data indicate that the surgical creation of a left-sided unilateral varicocele in the laboratory rat leads to a prompt and sustained diminution in the biosynthesis of T in both testes, and this effect seems to be primarily at the 17,20-desmolase step. This indicates that the bilateral anti-spermatogenic effect that occurs in the rat as a result of an experimental, unilateral varicocele may include a mechanism that involves defective Tproduction in the testis.