Does melatonin protect fetal brain during maternal hypothyroidism? An experimental study

To study the effects of melatonin in preventing neonatal neuronal apoptosis induced by maternal hypothyroidism.

Twelve healthy female Wistar rats, 12-16 weeks, were divided equally into three groups. Group-A was labelled as control. Group-B was made hypothyroid by giving 15mg/kg of propylthiouracyl (PTU) daily whereas Group-C was given PTU along with melatonin (10mg of melatonin/kg/day) in drinking water. After one week of treatment, the female rats were allowed to mate and conceive. The treatment of all groups continued throughout the period of pregnancy and lactation. After delivery, a total of 30 pups, 10 from each group, were labelled and sacrificed on 22nd day of life. The serum levels of TSH, T3 and T4 of the pups were measured. The brains were extracted from the skull and homogenized for isolation of mitochondria to determine the levels of cytochrome c oxidase and for isolation of RNAs to measure the levels of gene expressions of caspases 3, 9 and 8.

Group-B pups showed a significant increase in serum levels of TSH (21 ± 3.7 mg/dl), and gene expression levels of caspase 3 (0.85±0.02) and 9 (0.69±0.02) where as in Group-C, there was visible reduction in concentration of TSH (15 ± 2.4 mg/dl), caspase 3 (0.50±0.02) and 9 (0.25±0.01) expressions. Increase in cytochrome c oxidase enzyme concentration (3.416 ± 0.001) in Group-B was the result of mitochondrial outer membrane rupture, causing decrease in the number of neurons by accelerating apoptosis. A decrease in its level in Group-C (2.100 ± 0.001) indicated inhibition of apoptosis.

Intake of melatonin during pregnancy and lactation protected the brains of offspring from extensive apoptosis during maternal hypothyroidism.