Mature porcine sperm preserved in the cauda epididymis are quiescent. At ejaculation, they are mixed with the seminal vesicle fluid containing HCO3- and are rapidly activated. The role of HCO3- on the sperm activation process at ejaculation was studied in vitro. HCO3- quickly increased the motility, respiration rate and cAMP content of the porcine epididymal sperm. The extent of activation was proportional to the pCO2 in the medium. The activating effect of HCO3- on the motility was observed even in the absence of fructose as well as in the presence of KCN. 8-Bromoadenosine 3',5'-cyclic monophosphate and theophylline showed similar activating effects to that of HCO3-. However, HCO3(-)-free seminal plasma, Ca2+, amino acids, intermediates of the Krebs cycle, substrates of respiration and increases in the intracellular pH, extracellular pH or ionic strength of the medium had no effect. Fructose sustained the active state of the sperm and gradually increased both the motility and respiration rate when the dose of HCO3- was low. The anion channel blocker enhanced the activating effect of HCO3-. These results suggest that, upon ejaculation, HCO3- is a unique activator in vivo which makes the quiescent sperm motile via the HCO3(-)-adenylate cyclase-cAMP system, to which an endogenous HCO3- derived from metabolic CO2 may be related.
"Seminal vesicles are the male accessory sexual organs which function to secrete fluid that forms the last fraction of the ejaculate . Seminal fluid is rich in fructose  and contains electrolytes such as Cl À and HCO 3 À , where the latter plays important role in sperm activation . Seminal fluid is alkaline, with the pH reported around 7.54 in humans . "
[Show abstract][Hide abstract] ABSTRACT: Secretions of chloride (Cl(-))- and bicarbonate (HCO3(-))-rich fluid by the seminal vesicles could involve cystic fibrosis transmembrane regulator (CFTR), which activity can be stimulated by cAMP generated from the reaction involving adenylate cyclase (AC). In this study, we investigated levels of CFTR, AC, and cAMP in the seminal vesicles under testosterone influence. Orchidectomized adult male rats received 7-day treatment with 125 or 250 μg/kg/day of testosterone with or without flutamide or finasteride. At the end of the treatment, animals were sacrificed and seminal vesicles were harvested for analyses of CFTR and AC protein expression level by Western blotting. Distribution of CFTR and AC in seminal vesicles was observed by immunohistochemistry. Levels of cAMP and dihydrotestosterone in seminal vesicle homogenates were measured by ELISA. Cystic fibrosis transmembrane regulator, AC, and cAMP levels increased with increasing doses of testosterone (P < 0.05 compared to nontreated orchidectomized rats). Cystic fibrosis transmembrane regulator and AC were expressed at the apical membrane of the epithelium lining the seminal vesicle lumen with higher expression levels observed in testosterone-treated rats than in non-treated orchidectomized rats (P < 0.05). The inhibitory effects of flutamide or finasteride on these parameters were greater in 250 μg/kg/day testosterone-treated rats than their effects in 125 μg/kg/day testosterone-treated rats. Higher dihydrotestosterone levels were observed in seminal vesicle homogenates after treatment with 250 μg/kg/day than with 125 μg/kg/day of testosterone (P < 0.05). Increased levels of CFTR, AC, and cAMP in seminal vesicles might contribute toward an increase in Cl(-) and HCO3(-) concentrations in the seminal fluid as reported under testosterone influence.
"It has been known for more than sixty years that the luminal fluid of the female reproductive tract has a HCO 3 À content two to four times higher than that of the plasma (Vishwakarma, 1962; Murdoch and White, 1968; Maas et al., 1977). It is also known that HCO 3 À is essential to a number of reproductive events occurring in the female reproductive tract (Chan et al., 2006, 2009, 2012; Liu et al., 2012), including sperm motility (Mann and Lutwak-Mann, 1982; Tajima et al., 1987; Jones and Murdoch, 1996; Abaigar et al., 1999; Holt and Harrison, 2002; Wennemuth et al., 2003; Wennemuth, 2004; Mannowetz et al., 2011), capacitation (Boatman and Robbins, 1991; Shi and Roldan, 1995; Zhou et al., 2005), a sperm activation process by which sperm acquire their ability to fertilise the egg, and early embryo development (Chen et al., 2010; Lu et al., 2012). The questions as to how HCO 3 À is secreted into the lumen of the female reproductive tract and how HCO 3 À is transported into sperm and embryo have not been fully addressed. "
[Show abstract][Hide abstract] ABSTRACT: The solute carrier 26 (SLC26) family emerges as a distinct class of anion transporters with its members SLC26A3 (Slc26a3) and SLC26A6 (Slc26a6) reported to be electrogenic Cl(-) /HCO3 (-) exchangers. While it is known that uterine fluid has high HCO3 (-) content and that HCO3 (-) is essential for sperm capacitation, the molecular mechanisms underlying the transport of HCO3 (-) across uterine epithelial cells and sperm have not been fully investigated. The present review re-examines the results from early reports studying anion transport, finding clues for the involvement of Cl(-) /HCO3 (-) anion exchanges in electrogenic HCO3 (-) transport across endometrial epithelium. We also summarize recent work on Slc26a3 and Slc26a6 in uterine epithelial cells and sperm, revealing their functional role in working closely with the cystic fibrosis transmembrane conductance regulator (CFTR) for HCO3 (-) transport in these cells. The possible involvement of these anion exchangers in other HCO3 (-) dependent reproductive processes and their implications for infertility are also discussed.
Cell Biology International 01/2014; 38(1). DOI:10.1002/cbin.10183 · 1.93 Impact Factor
"During the epididymal maturation process in vivo, cyclic phosphodiesterase level of goat sperm decreases sharply [Jaiswal and Majumder, 1996] showing thereby that the sperm motility induction is associated with downregulation of cyclic phosphodiesterase activity resulting in decrease of the breakdown of cyclic-AMP which is essential for sperm forward motility [Jaiswal and Majumder, 1998; Okamura et al., 1985; Tajima et al., 1987; Rojas et al., 1992; Garbers and Kopf, 1980; Yeung , 1984; Vijayraghavan et al., 1985]. It is still not clear as to how the FMSF-receptor interaction triggers the flagellar motility. "
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