Further evidence for an inhibitory effect of L-tryptophan loading on testicular functions of rat.

Quantitative analysis of spermatogenesis at stage VII of the cycle of the seminiferous epithelium, radioimmunoassay of plasma testosterone and spectrofluorometric assay of brain 5-hydroxytryptamine (5-HT) levels were performed following administration of L-tryptophan (LT) alone and in Carbidopa pretreated Wistar strain rats. Carbidopa, an inhibitor of peripheral L-aromatic amino acid decarboxylase, was used to prevent the peripheral conversion of LT to 5-HT. The rats were sacrificed in groups on the day after (8th day) and 13 days after (21st day) the cessation of 7 days of treatment. The time duration of 13 days is approximately equivalent to one cycle of the seminiferous epithelium in Wistar strain rats. LT enhanced the brain 5-HT level, the increase being much greater in Carbidopa plus LT treated rats. However, reduction of plasma testosterone was similar in both the treated groups. There was no significant change in count of the germ cells on the day after cessation of treatment. However, marked degeneration of step 7 spermatids was observed when the analysis was performed 13 days after cessation of treatment. Human chorionic gonadotropin (HCG) administration along with Carbidopa plus LT treatment partially prevented the step 7 spermatid degeneration. These findings suggest that the inhibition of spermatogenesis and steroidogenesis following LT administration was secondary to decreased pituitary gonadotropin secretion which is in turn under the influence of brain 5-HT neurones. There is a minimum possibility of a direct action of LT, after conversion to 5-HT, on testicular tissue.