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.