Abstract

BackgroundDegenerative effects of critical regulators of reproduction, the kisspeptin peptides, on cellular aspects of sexually immature male gonads are known but similar information on accessory sex glands remain elusive.MethodsPrepubertal laboratory rats were injected kisspeptin-10 at three different dosage concentrations (10 pg, 1 ng and 1 microgram) for a period of continuous 12 days at the rate of two doses per day. Control rats were maintained in parallel. The day following the end of the experimental period, seminal vesicles were removed and processed for light and electron microscopic examination using the standard methods. DNA damage was estimated by DNA ladder assay and DNA fragmentation assay.ResultsThe results demonstrated cellular degeneration. Epithelial cell height of seminal vesicles decreased significantly at all doses (P < 0.05). Marked decrease in epithelial folds was readily noticeable, while the lumen was dilated. Ultrastructural changes were characterized by dilatation of endoplasmic reticulum and Golgi complex, heterochromatization of nuclei, invagination of nuclear membranes and a decreased number of secretory granules. Percent DNA damage to the seminal vesicle was 19.54 +/- 1.98, 38.06 +/- 2.09 and 58.18 +/- 2.59 at 10 pg, 1 ng and 1 microgram doses respectively.ConclusionThe study reveals that continuous administration of kisspeptin does not lead to an early maturation but instead severe degeneration of sexually immature seminal vesicles.

Highlights

  • Degenerative effects of critical regulators of reproduction, the kisspeptin peptides, on cellular aspects of sexually immature male gonads are known but similar information on accessory sex glands remain elusive

  • Kisspeptin-54 was originally identified as metastasis suppresser peptide from malignant melanoma cells that had been suppressed for metastatic potential by the introduction of human chromosome 6, named metastin [2,3,4]

  • The pseudostratified epithelium of secretory acinus rested on thin basement membrane highly folded to form irregular crypts and peaks

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Summary

Introduction

Degenerative effects of critical regulators of reproduction, the kisspeptin peptides, on cellular aspects of sexually immature male gonads are known but similar information on accessory sex glands remain elusive. In 1999, Lee and colleagues discovered in the rat a novel G protein-coupled receptor, the GPR54. The GPR54 gene encodes a G protein-coupled receptor [1]. It was later shown to mediate the actions of a unique family of KiSS-1 derived endogenous ligands known as kisspeptins. The KiSS-1 gene encodes a 145-amino acid peptide that is cleaved into an amidated C-terminal 54 amino acid product, kisspeptin or metastin. Kisspeptin-54 was originally identified as metastasis suppresser peptide from malignant melanoma cells that had been suppressed for metastatic potential by the introduction of human chromosome 6, named metastin [2,3,4].

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