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Introduction: Preeclampsia is the principal cause of maternal morbidity and is characterized by hypertension, proteinuria, and edema. It is believed that oxidative stress plays an essential role in the pathophysiology of preeclampsia. This study was conducted to determine the effect of tempol on fetal limb hemorrhage, malformations, and oxidative stress in an N-nitro-L-arginine methyl ester (L-NAME)-induced preeclamptic rat model.
Methods: To induce preeclampsia, L-NAME (50 mg/kg/day, oral) was administered from day 11 of pregnancy to day 22. Four preeclamptic groups received L-NAME alone, L-NAME+tempol (20, 60, 180 mg/kg/day; (L-NAME, L-T20, L-T60, L-T180 groups, respectively). The control group (normal pregnant) received only tap water, and the T60 group received tempol (60 mg/Kg) alone (without L-NAME). The concentration of 8-isoprostane in plasma and placenta, number and weight of the fetuses, and the limb defects were measured on the 22ndday of the pregnancy. Results: L-NAME administration caused placental oxidative stress, limb defects and hemorrhage, and low fetal weight. Administration of tempol at 20 and 60 mg/kg/day reduced limb defects (10.5 and 7.2 percent versus 24.7 percent) and limb hemorrhage (14.5 and 9.5 percent versus 23 percent) induced by L-NAME. After administration of tempol (20 and 60 mg/kg), fetal weight increased (5.14±0.08 and 5.44±0.15 versus 4.27± 0.11 g). Administration of tempol at the high dose (180 mg/kg/day) did not produce any significant effects on the measured parameters.
Conclusion: Tempol with certain doses improves fetal outcomes in an experimental rat model of preeclampsia. These may be the results of its antioxidant action.

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