Article ID Journal Published Year Pages File Type
2600054 Toxicology Letters 2011 7 Pages PDF
Abstract

Perfluorinated compounds (PFCs) comprise a large class of man-made chemicals of which some are persistent and present throughout the ecosystem. This raises concerns about potential harmful effects of such PFCs on humans and the environment. In order to investigate the effects of potentially harmful PFCs on steroid hormone production, human adrenocortical H295R cells were exposed to three persistent PFCs including perfluorooctane sulfonate (PFOS), perfluorooctanoic acid (PFOA) and perfluorononanoic acid (PFNA) at six different concentrations (6 nM to 600 μM) for 48 h. Exposure to 600 μM PFOS resulted in a dose-responsive increase in oestradiol as well as a smaller dose-responsive increase in progesterone and testosterone secretion measured using radioimmunoassay. The aromatase activity was not significantly altered by PFOS. Only small changes in hormone secretion were detected following exposure to PFOA and PFNA. Gene expression of CYP11A, quantified using qRT-PCR was decreased by all exposure doses of PFOA, whereas HMGR expression was decreased by 60 nM PFNA. The viability markedly decreased by exposure to 600 μM of PFOA or PFNA, but not PFOS. Flow cytometric analysis demonstrated a significant increase in apoptosis following exposure to PFNA at the highest concentration. We conclude that PFOS is capable of altering steroidogenesis in the H295R in vitro model by a mechanism other than changes in gene expression or activity of aromatase. Additionally, PFCs appear to differentially affect cell viability with induction of cell death via apoptosis at high doses of PFNA.

► We investigate steroid secretion, gene expression and cell cycle alterations in H295R cells exposed to PFOS, PFOA and PFNA. ► High dose of PFOS alters oestradiol secretion in vitro. ► This takes place without changes in aromatase activity or expression of CYP19. ► High doses of PFNA induces cell death by apoptosis.

Related Topics
Life Sciences Environmental Science Health, Toxicology and Mutagenesis
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