Oscopic examination using the standard methods. DNA damage was estimated by
Oscopic examination using the standard methods. DNA damage was estimated by DNA ladder assay and DNA fragmentation assay. Results: The 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. Conclusion: The study reveals that continuous administration of kisspeptin does not lead to an early maturation but instead severe degeneration of sexually immature seminal vesicles.Background 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 PubMed ID:https://www.ncbi.nlm.nih.gov/pubmed/28506461 cleaved into an amidated C-terminal 54 amino acid product, kisspeptin or metastin. Shorter fragments of kisspeptin-54, the kisspeptin-14, kisspeptin-13, and kisspeptin-10, also bind to GPR54. 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, hence named metastin [2-4]. In* Correspondence: [email protected] 1 Gomal Centre of Biochemistry and Biotechnology, Gomal University, Dera Ismail Khan 29050, Pakistan Full list of author information is available at the end of the article2003 two independent groups showed that dysfunctional or deletional mutations in the gene encoding the G protein-coupled receptor, GPR54, cause hypogonadotropic hypogonadism, a condition characterized by absent or delayed pubertal development in humans and mice [5,6]. Kisspeptin secreting neurons are found in the arcuate nucleus (Arc), the periventricular nucleus (PeN), and the anteroventral periventricular PubMed ID:https://www.ncbi.nlm.nih.gov/pubmed/27663262 nucleus (AVPV) in mice [7-9]. Expression of both KiSS-1 and GPR54 mRNA is regulated developmentally as well as hormonally, with a sharp increase at prepubertal age in both male and female rats, changes throughout the estrous cycle in adult females, and increases after gonadectomy that is prevented by sex steroid replacement in both males and females [10,11]. Kisspeptin potently release LH in mice and rats, in both males and females, and in prepubertal, pubertal, and adult rats, as well as in juvenile agonadal male monkeys [7,10,12,13].?2012 Ramzan et al; licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.Ramzan et al. Reproductive Biology and Endocrinology 2012, 10:18 http://www.rbej.com/content/10/1/Page 2 ofWhen kisspeptin acts at the level of the hypothalamus to increase GnRH secretion, it produces an increase in LH release from the pituitary. However, some order NSC309132 studies suggest that kisspeptin may also act at the level of the pituitary to evoke LH secr.