Antenatal antioxidant treatment with melatonin to decrease newborn neurodevelopmental deficits and brain injury caused by fetal growth restriction.
Study Goal
The researchers aimed to determine whether maternal antenatal melatonin administration could reduce brain injury and improve neurological function in fetal intrauterine growth restriction (IUGR) in an ovine model and later in a pilot human clinical trial.
Results Summary
Melatonin administration reduced oxidative stress, normalized myelination, and improved axonopathy in IUGR lamb brains, leading to significant functional improvements. In the human pilot trial, melatonin reduced placental oxidative stress without adverse maternal or fetal effects.
Population
Pregnant sheep (ovine model) and women with an IUGR fetus (human pilot trial).
Effective Dosage
Not specified (intravenous infusion in sheep, oral administration in humans).
Duration
Until term in sheep; duration in humans not specified.
Interactions
None mentioned
| Intervention | Direction | Endpoint | Population | Dosage | Impact | Claim # |
|---|---|---|---|---|---|---|
maternal antenatal melatonin administration | decrease | brain injury | ovine IUGR | - | reduced | #1 |
- | increase | achieving normal neonatal lamb behaviors, such as standing and suckling | IUGR lambs | - | took significantly longer | #2 |
- | increase | widespread cellular and axonal lipid peroxidation, and white matter hypomyelination and axonal damage | IUGR brains | - | showed | #3 |
maternal melatonin administration | decrease | oxidative stress | IUGR lamb brains | - | ameliorated | #4 |
maternal melatonin administration | increase | myelination | IUGR lamb brains | - | normalized | #5 |
maternal melatonin administration | decrease | axonopathy | IUGR lamb brains | - | rescued | #6 |
maternal melatonin administration | decrease | time to attach to and suckle at the udder after birth | IUGR + MLT lambs | - | demonstrated significant functional improvements including a reduced time taken | #7 |
oral melatonin administration | no change | adverse maternal or fetal effects | women with an IUGR fetus | - | was not associated with adverse maternal or fetal effects | #8 |
maternal melatonin | decrease | oxidative stress, as evidenced by reduced malondialdehyde levels | IUGR + MLT placenta | - | significantly reduced | #9 |
Fetal intrauterine growth restriction (IUGR) is a serious pregnancy complication associated with increased rates of perinatal morbidity and mortality, and ultimately with long-term neurodevelopmental impairments. No intervention currently exists that can improve the structure and function of the IUGR brain before birth. Here, we investigated whether maternal antenatal melatonin administration reduced brain injury in ovine IUGR. IUGR was induced in pregnant sheep at 0.7 gestation and a subset of ewes received melatonin via intravenous infusion until term. IUGR, IUGR + melatonin (IUGR + MLT) and control lambs were born naturally, neonatal behavioral assessment was used to examine neurological function and at 24 hr after birth the brain was collected for the examination of neuropathology. Compared to control lambs, IUGR lambs took significantly longer to achieve normal neonatal lamb behaviors, such as standing and suckling. IUGR brains showed widespread cellular and axonal lipid peroxidation, and white matter hypomyelination and axonal damage. Maternal melatonin administration ameliorated oxidative stress, normalized myelination and rescued axonopathy within IUGR lamb brains, and IUGR + MLT lambs demonstrated significant functional improvements including a reduced time taken to attach to and suckle at the udder after birth. Based on these observations, we began a pilot clinical trial of oral melatonin administration to women with an IUGR fetus. Maternal melatonin was not associated with adverse maternal or fetal effects and it significantly reduced oxidative stress, as evidenced by reduced malondialdehyde levels, in the IUGR + MLT placenta compared to IUGR alone. Melatonin should be considered for antenatal neuroprotective therapy in human IUGR.