Creation of both gametes, sperm and oocyte, and their fusion during fertilization are essential step for beginning of life. Although molecular mechanisms regulating gametogenesis, fertilization, and early embryonic development are still subjected to intensive study, a lot of phenomena remain unclear. Based on our best knowledge and own results, we consider gasotransmitters to be essential for various signalisation in oocytes and embryos. In accordance with nitric oxide (NO) and hydrogen sulfide (H2S) physiological necessity, their involvement during oocyte maturation and regulative role in fertilization followed by embryonic development have been described. During these processes, NO- and H2S-derived posttranslational modifications represent the main mode of their regulative effect. While NO represent the most understood gasotransmitter and H2S is still intensively studied gasotransmitter, appreciation of carbon monoxide (CO) role in reproduction is still missing. Overall understanding of gasotransmitters including their interaction is promising for reproductive medicine and assisted reproductive technologies (ART), because these approaches contend with failure of in vitro assisted reproduction.

• MeSH
• Reproductive Techniques, Assisted * MeSH
• Gametogenesis physiology   MeSH
• Gasotransmitters metabolism   physiology   MeSH
• Humans MeSH
• Oocytes metabolism   physiology   MeSH
• Nitric Oxide metabolism   physiology   MeSH
• Carbon Monoxide metabolism   physiology   MeSH
• Protein Processing, Post-Translational MeSH
• Hydrogen Sulfide metabolism   MeSH
• Animals MeSH
• Check Tag
• Humans MeSH
• Male MeSH
• Female MeSH
• Animals MeSH
• Publication type
• Journal Article MeSH
• Review MeSH
• Names of Substances
• Gasotransmitters MeSH
• Nitric Oxide MeSH
• Carbon Monoxide MeSH
• Hydrogen Sulfide MeSH

Nitric oxide (NO) is identified as a signaling molecule involved in many cellular or physiological functions including meiotic maturation and parthenogenetic activation of mammalian oocytes. We observed that nitric oxide donor SNAP was potent to induce parthenogenetic activation in Xenopus eggs. NO-scavenger CPTIO impaired the effects of SNAP, providing evidence for the effects of the latter to be specific upon NO release. In Xenopus eggs, SNAP treatment induced pigment rearrangement, pronucleus formation and exocytosis of cortical granules. At a biochemical level, SNAP exposure lead to MAPK and Rsk inactivation within 30 minutes whereas MPF remained active, in contrast to calcium ionophore control where MPF activity dropped rapidly. MAPK inactivation could be correlated to pronuclear envelope reformation observed. In SNAP-treated eggs, a strong increase in intracellular calcium level was observed. NO effects were impaired in calcium-free or calcium limited medium, suggesting that that parthenogenetic activation of Xenopus oocytes with a NO donor was mainly calcium-dependent.

• MeSH
• Enzyme Activation drug effects   MeSH
• Spindle Apparatus drug effects   metabolism   MeSH
• Benzoates pharmacology   MeSH
• Nitric Oxide Donors pharmacology   MeSH
• Maturation-Promoting Factor metabolism   MeSH
• Imidazoles pharmacology   MeSH
• Kinetics MeSH
• Mitogen-Activated Protein Kinases metabolism   MeSH
• Morphogenesis drug effects   MeSH
• Ovum cytology   drug effects   metabolism   MeSH
• Nitric Oxide metabolism   MeSH
• Parthenogenesis MeSH
• Progesterone pharmacology   MeSH
• S-Nitroso-N-Acetylpenicillamine pharmacokinetics   MeSH
• Calcium metabolism   MeSH
• Xenopus laevis metabolism   MeSH
• Animals MeSH
• Check Tag
• Female MeSH
• Animals MeSH
• Publication type
• Journal Article MeSH
• Research Support, Non-U.S. Gov't MeSH
• Names of Substances
• 1,3-dihydroxy-4,4,5,5-tetramethyl-2-(4-carboxyphenyl)tetrahydroimidazole MeSH Browser
• Benzoates MeSH
• Nitric Oxide Donors MeSH
• Maturation-Promoting Factor MeSH
• Imidazoles MeSH
• Mitogen-Activated Protein Kinases MeSH
• Nitric Oxide MeSH
• Progesterone MeSH
• S-Nitroso-N-Acetylpenicillamine MeSH
• Calcium MeSH