Acute effects of hexabromocyclododecane on Leydig cell cyclic nucleotide signaling and steroidogenesis in vitro. Fa, S., Pogrmic-Majkic, K., Dakic, V., Kaisarevic, S., Hrubik, J., Andric, N., Stojilkovic, S. S, & Kovacevic, R. Toxicology letters, 218(1):81–90, March, 2013. ![Acute effects of hexabromocyclododecane on Leydig cell cyclic nucleotide signaling and steroidogenesis in vitro. [link]](https://bibbase.org/img/filetypes/link.svg "link")
Paper doi abstract bibtex Hexabromocyclododecane (HBCDD), an additive brominated flame retardant routinely added to various consumer products, was reported to have toxic effects upon biota, including endocrine disruption. In this study, the potential toxicity of HBCDD was tested in peripubertal rat Leydig cells in vitro during 6h exposure. HBCDD inhibited human chorionic gonadotropin- and forskolin-supported cAMP accumulation and steroidogenesis. It also inhibited basal cAMP production, but elevated basal steroidogenesis. The expression of several cAMP-dependent genes, including steroidogenic acute regulatory protein, cholesterol side chain cleavage enzyme, and 3β-hydroxysteroid dehydrogenase, was also inhibited by HBCDD treatment. Nevertheless, this was not accompanied by a decrease in steroidogenic acute regulatory protein expression, as documented by western blot analysis, and activity of steroidogenic enzymes, as documented by unaffected steroidogenesis in the presence of permeable 22(R)-hydroxycholesterol. However, HBCDD caused significant decrease in mitochondrial membrane potential in untreated and human chorionic gonadotropin-treated cells. This indicates that HBCDD acute toxicity in Leydig cells reflects changes in mitochondrial membrane potential-dependent cAMP production and basal and cAMP-regulated cholesterol transport. This in turn facilitates basal but inhibits cAMP-dependent steroidogenesis. Acute effects of HBCDD treatment on transcription are also indicative of its sustained effects on Leydig cell function.
@article{fa_acute_2013,
title = {Acute effects of hexabromocyclododecane on {Leydig} cell cyclic nucleotide signaling and steroidogenesis in vitro.},
volume = {218},
issn = {1879-3169},
url = {http://www.ncbi.nlm.nih.gov/pubmed/23347875},
doi = {10.1016/j.toxlet.2013.01.009},
abstract = {Hexabromocyclododecane (HBCDD), an additive brominated flame retardant routinely added to various consumer products, was reported to have toxic effects upon biota, including endocrine disruption. In this study, the potential toxicity of HBCDD was tested in peripubertal rat Leydig cells in vitro during 6h exposure. HBCDD inhibited human chorionic gonadotropin- and forskolin-supported cAMP accumulation and steroidogenesis. It also inhibited basal cAMP production, but elevated basal steroidogenesis. The expression of several cAMP-dependent genes, including steroidogenic acute regulatory protein, cholesterol side chain cleavage enzyme, and 3β-hydroxysteroid dehydrogenase, was also inhibited by HBCDD treatment. Nevertheless, this was not accompanied by a decrease in steroidogenic acute regulatory protein expression, as documented by western blot analysis, and activity of steroidogenic enzymes, as documented by unaffected steroidogenesis in the presence of permeable 22(R)-hydroxycholesterol. However, HBCDD caused significant decrease in mitochondrial membrane potential in untreated and human chorionic gonadotropin-treated cells. This indicates that HBCDD acute toxicity in Leydig cells reflects changes in mitochondrial membrane potential-dependent cAMP production and basal and cAMP-regulated cholesterol transport. This in turn facilitates basal but inhibits cAMP-dependent steroidogenesis. Acute effects of HBCDD treatment on transcription are also indicative of its sustained effects on Leydig cell function.},
number = {1},
journal = {Toxicology letters},
author = {Fa, Svetlana and Pogrmic-Majkic, Kristina and Dakic, Vanja and Kaisarevic, Sonja and Hrubik, Jelena and Andric, Nebojsa and Stojilkovic, Stanko S and Kovacevic, Radmila},
month = mar,
year = {2013},
pmid = {23347875},
keywords = {3-Hydroxysteroid Dehydrogenases, 3-Hydroxysteroid Dehydrogenases: genetics, 3-Hydroxysteroid Dehydrogenases: metabolism, Androgens, Androgens: analysis, Animals, Brominated, Brominated: toxicity, Cell Cycle, Cell Cycle: drug effects, Cell Cycle: physiology, Cells, Cholesterol Side-Chain Cleavage Enzyme, Cholesterol Side-Chain Cleavage Enzyme: genetics, Cholesterol Side-Chain Cleavage Enzyme: metabolism, Chorionic Gonadotropin, Chorionic Gonadotropin: antagonists \& inhibitors, Chorionic Gonadotropin: pharmacology, Conditioned, Conditioned: chemistry, Culture Media, Cultured, Cyclic AMP, Cyclic AMP: genetics, Cyclic AMP: metabolism, Cyclic GMP, Cyclic GMP: genetics, Cyclic GMP: metabolism, Dose-Response Relationship, Drug, Environmental Pollutants, Environmental Pollutants: toxicity, Flame Retardants: toxicity, Flame retardants, Forskolin, Forskolin: antagonists \& inhibitors, Forskolin: pharmacology, Gene Expression, Gene Expression: drug effects, Hydrocarbons, Leydig Cells, Leydig Cells: drug effects, Leydig Cells: metabolism, Male, Membrane Potential, Mitochondrial, Mitochondrial: drug effects, Mitochondrial: physiology, Nucleotides, Nucleotides: metabolism, Phosphoproteins, Phosphoproteins: genetics, Phosphoproteins: metabolism, Progesterone, Progesterone: analysis, Rats, Signal Transduction, Wistar},
pages = {81--90},
}
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HBCDD inhibited human chorionic gonadotropin- and forskolin-supported cAMP accumulation and steroidogenesis. It also inhibited basal cAMP production, but elevated basal steroidogenesis. The expression of several cAMP-dependent genes, including steroidogenic acute regulatory protein, cholesterol side chain cleavage enzyme, and 3β-hydroxysteroid dehydrogenase, was also inhibited by HBCDD treatment. Nevertheless, this was not accompanied by a decrease in steroidogenic acute regulatory protein expression, as documented by western blot analysis, and activity of steroidogenic enzymes, as documented by unaffected steroidogenesis in the presence of permeable 22(R)-hydroxycholesterol. However, HBCDD caused significant decrease in mitochondrial membrane potential in untreated and human chorionic gonadotropin-treated cells. 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Acute effects of HBCDD treatment on transcription are also indicative of its sustained effects on Leydig cell function.","number":"1","journal":"Toxicology letters","author":[{"propositions":[],"lastnames":["Fa"],"firstnames":["Svetlana"],"suffixes":[]},{"propositions":[],"lastnames":["Pogrmic-Majkic"],"firstnames":["Kristina"],"suffixes":[]},{"propositions":[],"lastnames":["Dakic"],"firstnames":["Vanja"],"suffixes":[]},{"propositions":[],"lastnames":["Kaisarevic"],"firstnames":["Sonja"],"suffixes":[]},{"propositions":[],"lastnames":["Hrubik"],"firstnames":["Jelena"],"suffixes":[]},{"propositions":[],"lastnames":["Andric"],"firstnames":["Nebojsa"],"suffixes":[]},{"propositions":[],"lastnames":["Stojilkovic"],"firstnames":["Stanko","S"],"suffixes":[]},{"propositions":[],"lastnames":["Kovacevic"],"firstnames":["Radmila"],"suffixes":[]}],"month":"March","year":"2013","pmid":"23347875","keywords":"3-Hydroxysteroid Dehydrogenases, 3-Hydroxysteroid Dehydrogenases: genetics, 3-Hydroxysteroid Dehydrogenases: metabolism, Androgens, Androgens: analysis, Animals, Brominated, Brominated: toxicity, Cell Cycle, Cell Cycle: drug effects, Cell Cycle: physiology, Cells, Cholesterol Side-Chain Cleavage Enzyme, Cholesterol Side-Chain Cleavage Enzyme: genetics, Cholesterol Side-Chain Cleavage Enzyme: metabolism, Chorionic Gonadotropin, Chorionic Gonadotropin: antagonists & inhibitors, Chorionic Gonadotropin: pharmacology, Conditioned, Conditioned: chemistry, Culture Media, Cultured, Cyclic AMP, Cyclic AMP: genetics, Cyclic AMP: metabolism, Cyclic GMP, Cyclic GMP: genetics, Cyclic GMP: metabolism, Dose-Response Relationship, Drug, Environmental Pollutants, Environmental Pollutants: toxicity, Flame Retardants: toxicity, Flame retardants, Forskolin, Forskolin: antagonists & inhibitors, Forskolin: pharmacology, Gene Expression, Gene Expression: drug effects, Hydrocarbons, Leydig Cells, Leydig Cells: drug effects, Leydig Cells: metabolism, Male, Membrane Potential, Mitochondrial, Mitochondrial: drug effects, Mitochondrial: physiology, Nucleotides, Nucleotides: metabolism, Phosphoproteins, Phosphoproteins: genetics, Phosphoproteins: metabolism, Progesterone, Progesterone: analysis, Rats, Signal Transduction, Wistar","pages":"81–90","bibtex":"@article{fa_acute_2013,\n\ttitle = {Acute effects of hexabromocyclododecane on {Leydig} cell cyclic nucleotide signaling and steroidogenesis in vitro.},\n\tvolume = {218},\n\tissn = {1879-3169},\n\turl = {http://www.ncbi.nlm.nih.gov/pubmed/23347875},\n\tdoi = {10.1016/j.toxlet.2013.01.009},\n\tabstract = {Hexabromocyclododecane (HBCDD), an additive brominated flame retardant routinely added to various consumer products, was reported to have toxic effects upon biota, including endocrine disruption. In this study, the potential toxicity of HBCDD was tested in peripubertal rat Leydig cells in vitro during 6h exposure. HBCDD inhibited human chorionic gonadotropin- and forskolin-supported cAMP accumulation and steroidogenesis. It also inhibited basal cAMP production, but elevated basal steroidogenesis. The expression of several cAMP-dependent genes, including steroidogenic acute regulatory protein, cholesterol side chain cleavage enzyme, and 3β-hydroxysteroid dehydrogenase, was also inhibited by HBCDD treatment. Nevertheless, this was not accompanied by a decrease in steroidogenic acute regulatory protein expression, as documented by western blot analysis, and activity of steroidogenic enzymes, as documented by unaffected steroidogenesis in the presence of permeable 22(R)-hydroxycholesterol. However, HBCDD caused significant decrease in mitochondrial membrane potential in untreated and human chorionic gonadotropin-treated cells. This indicates that HBCDD acute toxicity in Leydig cells reflects changes in mitochondrial membrane potential-dependent cAMP production and basal and cAMP-regulated cholesterol transport. This in turn facilitates basal but inhibits cAMP-dependent steroidogenesis. Acute effects of HBCDD treatment on transcription are also indicative of its sustained effects on Leydig cell function.},\n\tnumber = {1},\n\tjournal = {Toxicology letters},\n\tauthor = {Fa, Svetlana and Pogrmic-Majkic, Kristina and Dakic, Vanja and Kaisarevic, Sonja and Hrubik, Jelena and Andric, Nebojsa and Stojilkovic, Stanko S and Kovacevic, Radmila},\n\tmonth = mar,\n\tyear = {2013},\n\tpmid = {23347875},\n\tkeywords = {3-Hydroxysteroid Dehydrogenases, 3-Hydroxysteroid Dehydrogenases: genetics, 3-Hydroxysteroid Dehydrogenases: metabolism, Androgens, Androgens: analysis, Animals, Brominated, Brominated: toxicity, Cell Cycle, Cell Cycle: drug effects, Cell Cycle: physiology, Cells, Cholesterol Side-Chain Cleavage Enzyme, Cholesterol Side-Chain Cleavage Enzyme: genetics, Cholesterol Side-Chain Cleavage Enzyme: metabolism, Chorionic Gonadotropin, Chorionic Gonadotropin: antagonists \\& inhibitors, Chorionic Gonadotropin: pharmacology, Conditioned, Conditioned: chemistry, Culture Media, Cultured, Cyclic AMP, Cyclic AMP: genetics, Cyclic AMP: metabolism, Cyclic GMP, Cyclic GMP: genetics, Cyclic GMP: metabolism, Dose-Response Relationship, Drug, Environmental Pollutants, Environmental Pollutants: toxicity, Flame Retardants: toxicity, Flame retardants, Forskolin, Forskolin: antagonists \\& inhibitors, Forskolin: pharmacology, Gene Expression, Gene Expression: drug effects, Hydrocarbons, Leydig Cells, Leydig Cells: drug effects, Leydig Cells: metabolism, Male, Membrane Potential, Mitochondrial, Mitochondrial: drug effects, Mitochondrial: physiology, Nucleotides, Nucleotides: metabolism, Phosphoproteins, Phosphoproteins: genetics, Phosphoproteins: metabolism, Progesterone, Progesterone: analysis, Rats, Signal Transduction, Wistar},\n\tpages = {81--90},\n}\n\n","author_short":["Fa, S.","Pogrmic-Majkic, K.","Dakic, V.","Kaisarevic, S.","Hrubik, J.","Andric, N.","Stojilkovic, S. 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