Melatonin improves development of early mouse embryos impaired by actinomycin-D and TNF-α

Melatonin, a reactive oxygen species (ROS) scavenger and an antioxidant, has been shown that can inhibit apoptosis. Administration of melatonin may improve embryo development in assisted reproductive technology (ART).

The aim of this study was to evaluate the role of melatonin in inhibition of spontaneous and induced apoptosis by Tumor Necrosis Factor Alph (TNF-α) and actinomycin-D during preimplantation development of mouse embryos.

Female BALB/c mice were superovulated with pregnant mare serum gonadotropin (PMSG) followed by human chorionic gonadotropin (HCG), then allowed to mate with male mice. The resultant 2-cell embryos were divided into six groups as follows: control (group I), melatonin (group II), actinomycin-D (group III), actinomycin-D + melatonin (group IV), TNF-α (group V), and TNF-α + melatonin (group VI). We recorded the numbers and developmental rates of the 4-cell, 8-cell, morula and blastocyst embryos. Blastocysts were stained with acridine orange in order to assess for the embryo quality.

The group IV showed a significantly higher developmental rate of blastocysts compared to group III (p<0.05). The number of dead blastomers was significantly decreased in group IV in comparison to group III (p<0.05). Both V and VI groups had a lower developmental rate and lesser quality of blastocysts compared with group I. There was no significant difference in the developmental rate of blastocysts from group II compared to group I (p<0.05).

Supplementation of embryo culture media with melatonin can improve the quality and developmental rate of embryos. Melatonin can prevent cell death that was induced by TNF- α and actinomycine-D.