Abstract
Mammalian spermatozoa are not able to fertilize an egg immediately upon ejaculation. They acquire this ability during their transit through the female genital tract in a process known as capacitation. The mammalian oviduct acts as a functional sperm reservoir providing a suitable environment that allows the maintenance of sperm fertilization competence until ovulation occurs. After ovulation, spermatozoa are gradually released from the oviductal reservoir in the caudal isthmus and ascend to the site of fertilization. Capacitating-related changes in sperm plasma membrane seem to be responsible for sperm release from oviductal epithelium. Anandamide is a lipid mediator that participates in the regulation of several female and male reproductive functions. Previously we have demonstrated that anandamide was capable to release spermatozoa from oviductal epithelia by induction of sperm capacitation in bovines. In the present work we studied whether anandamide might exert its effect by activating the nitric oxide (NO) pathway since this molecule has been described as a capacitating agent in spermatozoa from different species. First, we demonstrated that 1 µM NOC-18, a NO donor, and 10 mM L-Arginine, NO synthase substrate, induced the release of spermatozoa from the oviductal epithelia. Then, we observed that the anandamide effect on sperm oviduct interaction was reversed by the addition of 1 µM L-NAME, a NO synthase inhibitor, or 30 µg/ml Hemoglobin, a NO scavenger. We also demonstrated that the induction of bull sperm capacitation by nanomolar concentrations of R(+)-methanandamide or anandamide was inhibited by adding L-NAME or Hemoglobin. To study whether anandamide is able to produce NO, we measured this compound in both sperm and oviductal cells. We observed that anandamide increased the levels of NO in spermatozoa, but not in oviductal cells. These findings suggest that anandamide regulates the sperm release from oviductal epithelia probably by activating the NO pathway during sperm capacitation.
Highlights
The mammalian oviduct acts as a functional sperm reservoir providing an environment that allows maintenance and competition for fertilization of the oocyte
To study the participation of the nitric oxide (NO) in the release of the spermatozoa from oviductal epithelia, co-cultures of bovine oviductal epithelial cells (BOEC) and sperm cells were incubated with increasing concentrations of NOC-18, a NO donor
Low or high concentrations did not exert any effect. To corroborate this result we analyzed whether L-Arginine, the NO synthases (NOS) substrate, might produce a similar effect
Summary
The mammalian oviduct acts as a functional sperm reservoir providing an environment that allows maintenance and competition for fertilization of the oocyte. Spermatozoa are sequestered in the lower region of the oviduct (isthmus) where they attach to epithelial cells. This event extends the sperm life, delaying sperm capacitation until ovulationassociated signals induce their release allowing the transit to the upper region of the oviduct (ampulla). Adherence to the oviduct plays a key role in the selection of spermatozoa. The binding and release of spermatozoa from the oviductal epithelium are modulated mainly by the sperm capacitation and only noncapacitated spermatozoa bind to oviductal cells [1,2]. Sperm capacitation includes a large number of structural and metabolic modifications such as an increase in intracellular ions and protein tyrosine phosphorylation, generation of reactive oxygen species and changes in metabolism, plasma membrane fluidity and motility [3,4]
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