Melatonin is a powerful scavenger of
oxygen free radicals. In humans,
melatonin is rapidly transferred from the maternal to the fetal circulation. To investigate whether or not maternal
melatonin administration can protect the fetal rat brain from radical-induced damage by increasing the activities of
antioxidant enzymes, we administered
melatonin to pregnant rats on day 20 of gestation.
Melatonin (10 mg/kg) was injected intraperitoneally at daytime (14:00 hr) and, to remove the fetuses, a
laparotomy was performed at 1, 2, or 3 hr after its administration. We measured the
melatonin concentration in the maternal serum and in fetal brain homogenates and determined the activities of
superoxide dismutase (SOD) and
glutathione peroxidase (GSH-Px) in fetal brain homogenates.
Melatonin administration markedly increased
melatonin concentrations in the maternal serum and fetal brain homogenates, with peak levels achieved 1 hr after
melatonin administration (serum: 538.2+/-160.7 pM/mL; brain homogenates: 13.8+/-2.8 pM/mg
protein). Between 1 and 3 hr after
melatonin administration, GSH-Px activity in fetal brain homogenates increased significantly (P<0.01). Similarly, SOD activity increased significantly between 1 and 2 hr after
melatonin administration (P<0.01). These results indicate that
melatonin administration to the mother increases
antioxidant enzyme activities in the fetal brain and may thereby provide indirect protection against
free radical injury. Thus,
melatonin may potentially be useful in the treatment of neurodegenerative conditions that may involve excessive
free radical production, such as
fetal hypoxia and
preeclampsia.