Jawerbaum A, Gonzalez E T, Novaro V, Faletti A, Gimeno M A
Centro de Estudios Farmacológicos y Botánicos, Consejo Nacional de Investigaciones Cientificas y Técnicas, Buenos Aires, Argentina.
Reprod Fertil Dev. 1998;10(2):185-90. doi: 10.1071/r97069.
Previous work described an increase in prostaglandin E (PGE) production by oocyte-cumulus complexes (OVA) obtained from non-insulin-dependent diabetic rats. More recently, it has been found that in control OVA nitric oxide (NO) mediates hCG-induced PGE secretion. To determine whether increases in PGE secretion by diabetic OVA are mediated by NO, the present study has evaluated the secretion of PGE by diabetic OVA, cultured in the absence or presence of hCG, NO donors (sodium nitroprusside (NP) and 3-morpholino-sydnonimine-hydrochloride (SIN-1)), and a NO synthase inhibitor (N(G)monomethyl-L-arginine; L-NMMA). hCG, NP and SIN-1 increased PGE secretion by diabetic OVA. L-NMMA did not modify basal secretion of PGE by control OVA but lowered PGE production in diabetic OVA to control values. L-NMMA prevented the hCG-induced PGE accumulation in control and diabetic OVA, and the quantities of PGE produced were similar to those of control OVA but lower than in diabetic OVA incubated in the absence of hCG. The effect of L-NMMA seems to be specific since N(G)monomethyl-D-arginine had no effect. NO synthase activity was higher in diabetic ovaries than in controls. The present results suggest that NO mediates the increased PGE production by diabetic OVA, probably a result of overproduction of NO.
先前的研究表明，从非胰岛素依赖型糖尿病大鼠获得的卵母细胞-卵丘复合体（OVA）中前列腺素E（PGE）的产生增加。最近发现，在对照OVA中，一氧化氮（NO）介导了人绒毛膜促性腺激素（hCG）诱导的PGE分泌。为了确定糖尿病OVA中PGE分泌的增加是否由NO介导，本研究评估了在无或有hCG、NO供体（硝普钠（NP）和盐酸3-吗啉代-西多胺（SIN-1））以及NO合酶抑制剂（N（G）-单甲基-L-精氨酸；L-NMMA）存在的情况下培养的糖尿病OVA中PGE的分泌。hCG、NP和SIN-1增加了糖尿病OVA中PGE的分泌。L-NMMA没有改变对照OVA中PGE的基础分泌，但将糖尿病OVA中PGE的产生降低至对照值。L-NMMA阻止了hCG诱导的对照和糖尿病OVA中PGE的积累，并且产生的PGE量与对照OVA相似，但低于在无hCG的情况下培养的糖尿病OVA。L-NMMA的作用似乎具有特异性，因为N（G）-单甲基-D-精氨酸没有作用。糖尿病卵巢中的NO合酶活性高于对照组。目前的结果表明，NO介导了糖尿病OVA中PGE产生的增加，这可能是NO产生过多的结果。
