Mercury impairs human primary endometrial stromal cell function†.

Abstract

Heavy metal exposures could compromise endometrial cells. Although studies assessed mercury toxicity in cell lines, limited data are available on the concentration of mercury that damage human endometrial stromal cells (hEnSCs) and alter endometrial function. This research aims to study the effects of mercury exposure on cell viability and functional features of hEnSCs. Primary hEnSCs were isolated from 23 endometrial biopsies obtained from healthy donors. After in vitro mercury exposure cell viability of hEnSCs was evaluated via tetrazolium salt metabolism and oxidative stress was assessed by 2', 7'-dichlorofluorescin diacetate assay. hEnSCs were decidualized in vitro in the presence of mercury (0, 25, 50, 75, 250, and 350 nM). Decidualization was evaluated based on prolactin and insulin-like growth factor-binding protein (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 reactive oxygen species production in hEnSCs after 24 h. Cell viability significantly decreased after 48 h and 72 h (P < 0.05) of mercury exposure at 500 nM. After in vitro decidualization and mercury treatment, decidual hEnSCs showed a dose-dependent decrease in prolactin and IGFBP1 secretion, particularly at 350 nM (P = 0.016). Cell proliferation was decreased in hEnSCs treated with 350 nM mercury (P < 0.001); an increase in apoptosis followed a dose-dependent trend in non-decidual and decidual hEnSCs. These findings support that mercury-induced damage could be due to an increase in ROS production.