the effect of nitric oxide on mouse pre-implantation embryo development and apoptosis

clinical studies have shown that in pathological conditions such as endometriosis and reproductive tract infection (male and female) there is an activation status of macrophages that produce large quantities of nitric oxide (no) in addition to other effector molecules. large amounts of no may have embryotoxic roles and produce infertility. this study was designed to evaluate the effect of different concentrations of no on mouse pre-implantation embryo development in vitro. mouse embryos (2-cell stage) were cultured in media containing different concentrations of sodium nitroprusside (snp), an no donor, or l-arginine methyl ester (l-name), an no syntase (nos) inhibitor. at the end of culture, cell apoptosis was studied by the terminal deoxynucleotidyl transferase-mediated dutp nick end-labeling (tunel) technique. the results showed that development of preimplantation embryos were inhibited by high concentration of snp (1 and 10 μm). in contrast, 0.1 μm of snp stimulated the embryo development. similarly, the inhibition of no by nos inhibitor resulted in the dose-dependent inhibition of embryo development, but the addition of 0.1 μm snp with l-name reversed the inhibitory effect of l-name. tunel technique showed that high concentration of no could induce apoptosis in the embryo, but at low concentration, it decreased apoptotic cell death