Jawerbaum A, Gonzalez E T, Carolina P, Debora S, Christian P, Gimeno M A
Centro de Estudios Farmacológicos y Botánicos, Consejo Nacional de Investigaciones Cientificas y Técnicas, Buenos Aires, Argentina.
Reprod Fertil Dev. 1999;11(2):105-10. doi: 10.1071/rd99033.
In the present work the prostaglandin E (PGE) production by ovulated, immature and in vitro matured oocyte-cumulus complexes (OCC) was evaluated in a rat model of type I diabetes induced by streptozotocin (60 mg kg(-1)). A diminished number of ovulated OCC were found in the type I diabetic rat. In contrast to the increment in PGE generation found previously in OCC and embryos from type II diabetic rats, it was found that PGE production by type I diabetic OCC was diminished in comparison with the controls. Nitric oxide synthase (NOS) activity is enhanced in proestrous ovaries from type I diabetic rats, but cGMP levels are diminished. SIN-1 (300 microM), a nitric oxide donor, significantly enhanced PGE generation by control OCC, but was unable to modify the PGE levels in type I diabetic OCC. L-NMMA, a nitric oxide inhibitor that diminished PGE values in type II diabetic OCC, did not modify PGE generation in either control and type I diabetic OCC. Superoxide dismutase (SOD, 1000 U mL(-1)), and SOD (1000 U mL(-1)) plus SIN-1 (300 microM), enhanced PGE generation by both control and diabetic OCC. The present results suggest that even when nitric oxide (NO) is overproduced in diabetic ovaries, the NO-PGE pathway is impaired in type I diabetic OCC. As SOD additions are able to increase PGE generation by diabetic OCC, high concentrations of free oxygen radicals might be quenching the NO, impairing its physiological functions.
在本研究中，在链脲佐菌素（60 mg kg⁻¹）诱导的I型糖尿病大鼠模型中，评估了排卵的、未成熟的以及体外成熟的卵母细胞-卵丘复合体（OCC）中前列腺素E（PGE）的产生情况。在I型糖尿病大鼠中发现排卵的OCC数量减少。与先前在II型糖尿病大鼠的OCC和胚胎中发现的PGE生成增加相反，发现I型糖尿病OCC产生的PGE与对照组相比减少。I型糖尿病大鼠动情前期卵巢中的一氧化氮合酶（NOS）活性增强，但cGMP水平降低。一氧化氮供体SIN-1（300 μM）显著增强了对照OCC产生的PGE，但无法改变I型糖尿病OCC中的PGE水平。一氧化氮抑制剂L-NMMA可降低II型糖尿病OCC中的PGE值，但对对照和I型糖尿病OCC中的PGE生成均无影响。超氧化物歧化酶（SOD，1000 U mL⁻¹）以及SOD（1000 U mL⁻¹）加SIN-1（300 μM）可增强对照和糖尿病OCC产生的PGE。目前的结果表明，即使糖尿病卵巢中一氧化氮（NO）产生过多，但I型糖尿病OCC中的NO-PGE途径仍受损。由于添加SOD能够增加糖尿病OCC产生的PGE，高浓度的游离氧自由基可能会淬灭NO，损害其生理功能。
