Abstract
Perfluorohexane sulfonate (PFHxS) is one of the most abundant perfluorinated compounds in the environment. Exposure to this compound has been correlated to a decrease in human fertility, although the molecular and cellular mechanisms underlying this correlation have not been described. The adverse reproductive effects of PFHxS could be based on alterations in oocyte maturation, the process rendering oocytes competent for fertilization. The aim of this study was to evaluate the effect of PFHxS on porcine oocyte viability and maturation in vitro, as well as on gap-junctional intercellular communication (GJIC) in cumulus–oocyte complexes (COCs), oocyte mitochondrial membrane potential (mΔΨ) and DNA damage in cumulus cells, as possible mechanisms of action. PFHxS caused cytotoxicity (medium lethal concentration, LC50 = 329.1 μM) and inhibition of oocyte maturation (medium inhibitory concentration, MIC50 = 91.68 μM). GJIC was not affected in exposed COCs. However, the mitochondrial membrane potential was significantly decreased in PFHxS-exposed oocytes at the germinal vesicle breakdown (GVBD) stage. In addition, exposure to PFHxS induced DNA damage in cumulus cells. Thus, inhibition of oocyte maturation by PFHxS could be attributed to a decreased oocyte mΔΨ at the GVBD and to DNA damage of the cumulus cells that support the oocyte.
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