The present study investigated the effect of nitric oxide (NO) on the lifes
pan of the corpus luteum (CL). Using a competitive nitric oxide synthase (N
OS) inhibitor, L-nitro arginine methyl ester (L-NAME, 600 mu mol/l), and a
long-life NO donor, diethyl-aminetriamine (DETA-NONOate, 10(-8), 10(-6) or
10(-4) mol/l), we found that in ovaries from rats at the mid stage of CL de
velopment, endogenous NO increased both glutathione (GSH) and progesterone
production. However, during prostaglandin F-2 alpha (PGF(2 alpha))-induced
luteolysis NO acted as an intermediary molecule in the inhibitory effect of
PGF(2 alpha), on GSH content. This was supported by the fact that in-vivo
PGF(2 alpha) treatment enhanced nitric oxide synthase (NOS) activity. These
results indicate that the NO could act with a dual action (protective or p
ro-oxidant) in CL development.