LAUSR

Heavy metal exposures could compromise endometrial cells and decidualization. Although studies assessed mercury toxicity in cell lines, limited data are available on the concentration of mercury that induces damage in hEnSC, which could alter endometrial function. This research aims to study effects of mercury exposure on cell viability and functional features of hEnSC. Primary hEnSC were isolated from 23 endometrial biopsies obtained from healthy egg donors. After in vitro mercury exposure or control treatment of hEnSC, cell viability was evaluated via tetrazolium salt metabolism and oxidative stress was assessed by 2',7'-DCFDA assay. hEnSC were decidualized in vitro in the presence of mercury (0, 25, 50, 75, 250 and 350 nM). Decidualization was evaluated based on prolactin and IGFBP1 secretion and cytoskeletal rearrangement (F-actin staining). Cell proliferation and apoptosis were evaluated by Ki67 immunostaining and TUNEL assay. Mercury doses of 250 nM (p = 0.028) and 500 nM (p = 0.026) increased ROS production in hEnSC after 24 h. Cell viability significantly decreased after 48 h and 72 h (p = 0.032 and p = 0.016, respectively) of mercury exposure at 500 nM. After in vitro decidualization and mercury treatment, decidual hEnSC showed a dose-dependent decrease in prolactin and IGFBP1 secretion, particularly at 350 nM (p = 0.016). Cell proliferation was decreased in hEnSC treated with 350 nM mercury (p < 0.001); an increase in apoptosis followed a dose-dependent trend in non-decidual and decidual hEnSC. These findings support that mercury-induced damage could be due to an increase in ROS production.