Melatonin protects against oxidative mitochondrial damage induced in rat placenta by ischemia and reperfusion

We assessed the effects of melatonin, a powerful scavenger of oxygen free r adicals, on ischemia/reperfusion-induced oxidative damage to mitochondria i n the rat placenta. In Wistar rats at day 19 of pregnancy, feto-placental i schemia was induced by occluding both utero-ovarian arteries for 20 min. Re perfusion was achieved by releasing the occlusion and restoring circulation for 30 min. Melatonin solution or the vehicle alone was injected intraperi toneally at dose of 10 mg/kg 1 hr before occlusion. Sham-ischemic animals w ere treated with vehicle. Each group consisted of 10 pregnant rats. We meas ured placental mitochondrial respiratory control index (RCI; a marker of mi tochondrial respiratory activity), the ratio of the added adenosine 5-dipho sphate (ADP) concentration to consumption of oxygen during state 3 respirat ion (ADP/O), and the concentration of thiobarbituric acid reactive substanc es (TBARS) in each group. RCI and ADP/O were significantly decreased by isc hemia/reperfusion, while TBARS were increased. Melatonin prevented these ch anges. These results indicate that exogenous melatonin protects against isc hemia/reperfusion-induced oxidative damage to mitochondria in rat placenta. Melatonin could be useful in treating preeclampsia and possibly other clin ical states involving excess free radical production, such as fetal growth restriction and fetal hypoxia.