Aluminum Chloride Causes the Dysfunction of Testes Through Inhibiting the ATPase Enzyme Activities and Gonadotropin Receptor Expression in Rats.

The aim of this experiment is to explore the effects of aluminum chloride (AlCl3) on the ATPase enzymes and gonadotropin receptors in the testes. Eighty male Wistar rats were orally exposed to 0 mg/kg body weight (BW) (control group, CG), 64 mg/kg BW (low-dose group, LG), 128 mg/kg BW (mid-dose group, MG), or 256 mg/kg BW (high-dose group, HG) for 120 days. The microstructure and ultrastructure of testes; the activities of Na+-K+-ATPase, Mg2+-ATPase, and Ca2+-ATPase; and the mRNA and protein expressions of follicle-stimulating hormone receptor (FSHR) and luteinizing hormone receptors (LHR) in the testes were examined. The results showed that the testes histological structure were damaged; the activities of Na+-K+-ATPase, Mg2+-ATPase, and Ca2+-ATPase, the mRNA and protein expressions of FSHR and LHR in the testes were all decreased in the rats with AlCl3 exposure. It indicates that AlCl3 causes the dysfunction of testes in rats.

Gonadotropin-inhibitory hormone and its receptor in the avian reproductive system.

Many hormones that are classified as neuropeptides are synthesized in vertebrate gonads in addition to the brain. Receptors for these hormones are also expressed in gonadal tissue; thus there is potential for a highly localized autocrine or paracrine effect of these hormones on a variety of gonadal functions. In the present study we focused on gonadotropin-inhibitory hormone (GnIH), a neuropeptide that was first discovered in the hypothalamus of birds. We present different lines of evidence for the synthesis of GnIH and its receptor in the avian reproductive system including gonads and accessory reproductive organs by studies on two orders of birds: Passeriformes and Galliformes. Binding sites for GnIH were initially identified via in vivo and in vitro receptor fluorography, and were localized in ovarian granulosa cells along with the interstitial layer and seminiferous tubules of the testis. Furthermore, species-specific primers produced clear PCR products of GnIH and GnIH receptor (GnIH-R) in songbird and quail gonadal and other reproductive tissues, such as oviduct, epididymis and vas deferens. Sequencing of the PCR products confirmed their identities. Immunocytochemistry detected GnIH peptide in ovarian thecal and granulosa cells, testicular interstitial cells and germ cells and pseudostratified columnar epithelial cells in the epididymis. In situ hybridization of GnIH-R mRNA in testes produced a strong reaction product which was localized to the germ cells and interstitium. In the epididymis, the product was also localized in the pseudostratified columnar epithelial cells. In sum, these results indicate that the avian reproductive system has the capability to synthesize and bind GnIH in several tissues. The distribution of GnIH and its receptor suggest a potential for autocrine/paracrine regulation of gonadal steroid production and germ cell differentiation and maturation.

Hypothalamic GnRH and pituitary gonadotroph relationships during rat fetal life.

The ontogeny of hypothalamic GnRH, of pituitary and gonadal receptors and of pituitary LH and FSH was studied in the fetal and neonatal rat. Hypothalamic, hypophyseal and gonadal primordia were dissected from animals ranging in age from postconceptual day 12 to birth. Immunoreactive GnRH was detectable in the hypothalamus from fetal day 12 onwards at a low level until day 17, whereafter hypothalamic GnRH content and concentration increased until birth. GnRH receptors were reliably detectable in the pituitary anlage from fetal day 16 onwards and increased progressively with advancing age whether expressed as content or concentration. Signs of pituitary LH synthesis were evident as early as fetal day 12 but intrapituitary LH levels remained low until fetal day 17 when levels increased progressively until the end of gestation. Pituitary FSH was undetectable until fetal day 19, thereafter rising dramatically until the end of gestation. GnRH binding to testicular and ovarian tissues was undetectable throughout the period of fetal development. The possible relations among the developmental changes in hypothalamic GnRH, pituitary GnRH receptors and gonadotrophins are discussed.