Abstract:
Previous work described an increase in prostaglandin E (PGE) production byoocyte-cumulus complexes (OVA) obtained from non-insulin-dependentdiabetic rats. More recently, it has been found that in control OVA nitricoxide (NO) mediates hCG-induced PGE secretion. To determine whether increasesin PGE secretion by diabetic OVA are mediated by NO, the present study hasevaluated the secretion of PGE by diabetic OVA, cultured in the absence orpresence of hCG, NO donors (sodium nitroprusside (NP) and3-morpholino-sydnonimine-hydrochloride (SIN-1)), and a NO synthaseinhibitor (N<emph type="7">G monomethyl-L-arginine; L-NMMA). hCG, NPand SIN-1 increased PGE secretion by diabetic OVA. L-NMMA did not modifybasal secretion of PGE by control OVA but lowered PGE production in diabeticOVA to control values. L-NMMA prevented the hCG-induced PGE accumulation incontrol and diabetic OVA, and the quantities of PGE produced were similar tothose of control OVA but lower than in diabetic OVA incubated in the absenceof hCG. The effect of L-NMMA seems to be specific sinceN<emph type="7">G monomethyl-D-arginine had no effect. NO synthaseactivity was higher in diabetic ovaries than in controls. The present resultssuggest that NO mediates the increased PGE production by diabetic OVA,probably a result of overproduction of NO.