Alterations of Testicular Function Induced by Hyperprolactinemia in the Rat

Abstract

The effects of hyperprolactinemia on testicular structure and pituitary-gonadal function were investigated in male rats. Hyperprolactinemia was induced in the Wistar-Furth rat by implantation of tissue fragments of a prolactin-secreting MtTW15 pituitary adenoma. The MtTW15 tissue was maintained in one animal group for 27 days (group A) and in another group for 37 days (group B). Appropriate age-matched controls were utilized in each study. Serum prolactin was significantly elevated (P less than 0.001) in both groups of MtTW15-bearing rats compared with their controls. The degree of hyperprolactinemia was more severe in rats of group B (2842 +/- 546 ng/ml) than in rats of group A (367 +/- 38 ng/ml). Accessory sex organ weights in group B rats were significantly lower than in controls, but were apparently unaffected in group A rats. Hyperprolactinemia induced definite but variable testicular alterations in both animal groups that presented as seminiferous epithelial disorganization, germ cell exfoliation, increased tubule wall thickness, and abnormal Leydig cell lipid content. Electron microscopy revealed structural disruption of Sertoli-germ cell junctional complexes and apical Sertoli cell cytoplasmic degeneration. The hyperprolactinemic rat exhibited significant reductions in serum luteinizing hormone (LH), testosterone (T), and androgen binding protein (ABP) when compared with controls. Eighty-six days following surgical removal of the MtTW15 tissue in a subgroup of group B rats, serum levels of prolactin and LH returned to normal, as did weights of accessory sex organs and testicular morphology. These results indicate that exposure to the MtTW15 adenoma and its later removal in the rat provides a workable model for studying the effects of hyperprolactinemia on testicular structure and function, and for identifying events involved in the subsequent recovery of spermatogenic disruption.

Evaluation of spermatozoa of the rat in hyperprolactinaemia induced by Metoclopramide

“…Our studies on the model of hyperprolactinaemia induced by MCP have confirmed information disclosed previously (Cameron et al, 1984;Katovich et al, 1985), namely that exfoliation of spermatogenic cells from the seminiferous tubules occurs. Our findings also confirmed previous observations that in hyperprolactinaemia, provoked by either MCP application or any other factors, the number of spermatozoa in the ejaculate is reduced (Segal et al, 1979;Rocco et al, 1983;Yousef et al, 1989).…”

Effects of hyperprolactinemia on testosterone production in rat Leydig cells

“…A homeostasis of plasma PRL is crucial for a normally functioning reproductive system. However, abnormally elevated plasma PRL levels for a long period of time are harmful for the gonadal functions [Katovich et al, 1985;Sharpe and McNeilly, 1980;Waeber et al, 1983].…”

Assessment of Circulating Hormones in Regulatory Toxicity Studies II. Male Reproductive Hormones

“…Prolactin regulates the number and sensitivity of LH receptors within Leydig cells. Although the evidence is not entirely uniform within a species, increased PRL concentrations have been generally reported to have suppressive effects on GnRH release, T levels, copulatory behavior, and degenerative effects on testicular spermatogenesis in many species, including the rat and man (Aleem et al 2005;Katovich et al 1985;Perryman and Thorner 1981). However, the opposite effect has been demonstrated in the mouse, with increased levels of gonadotropins (LH and FSH), increased copulatory behavior, and enlargement of ASOs (Bartke et al 1987;Wennbo et al 1997).…”