title: Effects of polar oil related hydrocarbons on steroidogenesis in vitro in H295R cells.
abstract: Oil pollution from various sources, including exploration, production and transportation, is a growing global concern. Of particular concern is the environmental impact of produced water (PW), the main waste discharge from oil and gas platforms. In this study, we have investigated the potential of polar hydrocarbon pollutants to disrupt or modulate steroidogenesis in vitro, using a human adrenocortical carcinoma cell line, the H295R assay. Effects of two of the major groups of compounds found in the polar fraction of crude oil and PW; alkylphenols (C(2)- and C(3)-AP) and naphthenic acids (NAs), as well as the polar fraction of PW as a whole has been assessed. Endpoints include hormone (cortisol, estradiol, progesterone, testosterone) production at the functional level and key genes for steroidogenesis (17β-HSD1, 17β-HSD4, 3β-HSD2, ACTHR, CYP11A1, CYP11B1, CYP11B2, CYP17, CYP19, CYP21, DAX1, EPHX, HMGR, SF1, STAR) and metabolism (CYP1A) at the molecular level. All compounds induced the production of both estradiol and progesterone in exposed H295R cells, while the C(3)-AP and NAs decreased the production of testosterone. Exposure to C(2)-AP caused an up-regulation of DAX1 and EPHX, while exposure to NAs caused an up-regulation of ACTHR. All compounds caused an up-regulation of CYP1A1. The results indicated that these hydrocarbon pollutants, including PW, have the potential to disrupt the vitally important process of steroidogenesis.
authors.affiliation: Department of Biology, University of Bergen, P.O. Box 7803, N-5020 Bergen, Norway. anne.knag@bio.uib.no
authors.forename: Anne Christine
authors.initials: AC
authors.lastname: Knag
authors.forename: Steven
authors.initials: S
authors.lastname: Verhaegen
authors.forename: Erik
authors.initials: E
authors.lastname: Ropstad
authors.forename: Ian
authors.initials: I
authors.lastname: Mayer
authors.forename: Sonnich
authors.initials: S
authors.lastname: Meier
mesh_terms: D002264:Carboxylic Acids / Q000737:chemistry / Q000633:toxicity; D045744:Cell Line, Tumor; D002470:Cell Survival / Q000187:drug effects; D019363:Cytochrome P-450 CYP1A1 / Q000235:genetics / Q000378:metabolism; D003577:Cytochrome P-450 Enzyme System / Q000235:genetics / Q000378:metabolism; D057137:DAX-1 Orphan Nuclear Receptor / Q000235:genetics / Q000378:metabolism; D004785:Environmental Pollutants / Q000737:chemistry* / Q000633:toxicity; D004851:Epoxide Hydrolases / Q000235:genetics / Q000378:metabolism; D004958:Estradiol / Q000378:metabolism; D006801:Humans; D006838:Hydrocarbons / Q000737:chemistry* / Q000633:toxicity; D006854:Hydrocortisone / Q000378:metabolism; D059392:Petroleum Pollution; D010636:Phenols / Q000737:chemistry / Q000633:toxicity; D011374:Progesterone / Q000378:metabolism; D012333:RNA, Messenger / Q000378:metabolism; D013256:Steroids / Q000378:metabolism*; D013739:Testosterone / Q000378:metabolism; D015854:Up-Regulation / Q000187:drug effects
chemical_list: D002264:Carboxylic Acids; D057137:DAX-1 Orphan Nuclear Receptor; D004785:Environmental Pollutants; D006838:Hydrocarbons; C539965:NR0B1 protein, human; D010636:Phenols; D012333:RNA, Messenger; D013256:Steroids; D013739:Testosterone; D011374:Progesterone; D004958:Estradiol; D003577:Cytochrome P-450 Enzyme System; D019363:Cytochrome P-450 CYP1A1; D004851:Epoxide Hydrolases; C522330:EPHX1 protein, human; D006854:Hydrocortisone; C046170:naphthenic acid