Abstract:
Nitric oxide (NO) regulation of ovarian function in mammals has been studied extensively. However,
relatively less information is available on NO action on meiotic G2-M1 transition in teleost oocytes. In the
present study using follicle-enclosed oocytes of Anabas testudineus, NO regulation of intra-oocyte
signaling events during meiotic G2-M1 transition were examined. Priming with NO donor, sodium
nitroprusside (SNP) prevented 17a,20b-dihydroxy-4-pregenen-3-one (17,20b-P)-induced germinal
vesicle break down (GVBD) in dose- and duration-dependent manner. Impaired GVBD response in SNPtreated
groups corroborated well with reduced p34Cdc2 (Thr161) phosphorylation. Immunoblot analysis
revealed that congruent with elevated cAMP-dependent protein kinase (PKA) phosphorylation (activation),
NO inhibition of meiotic maturation involves down regulation of Cdc25 activation, Mos synthesis
and MAPK3/1 (ERK1/2) phosphorylation. However, priming with PKA inhibitor (H89) could reverse SNP
attenuation of oocyte GVBD significantly. Collectively our results indicate that negative influence of NO
on meiotic G2-M1 transition in perch oocytes might involve PKA activation.
