Effect of peritoneal fluid on early embryonic \ndevelopment

The aetiology of endometriosis associated with infertility remains poorly \nunderstood. In recent years, the potential influence of peritoneal fluid (PF) or its \ncellular components have been proposed as possible mediators of infertility in \nendometriosis through it toxic effects on pre-implantation embryo. Several \nfactors have been identified as embryotoxic factors, however, the mechanism \nof embryotoxicity have not well clarified. Studies were therefore undertaken to \nclarify the possible mechanisms of embryotoxicity in endometriosis and to \ndetermine the possible embryotoxic factor(s) that involved in the process. The \nrole of exogenous nutrient (pyruvate) has also been examined in reducing or \neliminating the embryotoxicity. Peritoneal fluid was collected from infertile \nwomen at reproductive age with 21 endometriosis (PF-E) (7 minimal or mild, 7 \nmoderate, 7 severe) and 7 without endometriosis (PF-NE). Addition of PF-E to \nthe culture medium from all stages of endometriosis significantly suppressed \nthe mouse embryo growth at all stages of development, at 24, 48 and 72 hours, \nwhich correlated with the severity of the disease, as compared to control (no \nperitoneal fluid). Excessive pyruvate was able to reduce the embryotoxicity at \nall stages of development in minimal or mild and moderate PF-E, and only \nduring the first 24 hours in severe PF-E. The level of IL-6 concentration was \nsignificantly higher in PF-E as compared to PF-NE and correlated with the \nseverity of the disease. However, no significant difference was noted in the \nlevel of IL-8 between the two groups. Both interleukins were found to be \nembryotoxic with IL-6 is more potent. A positive correlation between the levels \nof IL-6 and its embryotoxicity was noted. These findings propose embryotoxicity \nto be a possible mechanism of infertility in endometriosis and the growth \npromoting effects of pyruvate indicated the mechanism of embryotoxicity might \ninvolve functional disruption of the intermediary metabolism such that \nexcessive pyruvate is required to maintain embryo growth. \nVl