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

ABSTRACT

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-alpha] 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-alpha [group V], and TNF-alpha + 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- alpha and actinomycine-D