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

Background: 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). Objective: 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-?) and actinomycin-D during preimplantation development of mouse embryos. Materials and Methods: 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-? (group V), and TNF-? + 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. Results: 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). Conclusion: 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- ? and actinomycine-D.