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• W2317702571 abstract "Vol. 124, No. 4 News | Science SelectionsOpen AccessUnexamined Endocrine Disruption? Pesticides Inhibit Prostaglandin Activityis accompanied byEffects of Common Pesticides on Prostaglandin D2 (PGD2) Inhibition in SC5 Mouse Sertoli Cells, Evidence of Binding at the COX-2 Active Site, and Implications for Endocrine Disruption Lindsey Konkel Lindsey Konkel Search for more papers by this author Published:1 April 2016https://doi.org/10.1289/ehp.124-A76Cited by:1View Article in:中文版AboutSectionsPDF ToolsDownload CitationsTrack Citations ShareShare onFacebookTwitterLinked InReddit Androgens are widely recognized as important drivers of male sexual development in the fetus.1 Some endocrine-disrupting chemicals have been shown to impact male sexual differentiation by affecting androgen production or blocking androgen receptors in target tissues.2 Comparatively little attention has been paid to the role that ubiquitous biologically active lipids called prostaglandins play in these developmental processes, although studies have found that prostaglandins help initiate male genital development.3,4,5 In this issue of EHP, researchers show that several structurally different endocrine-active pesticides suppress prostaglandin synthesis and signaling in mouse cells.6“The research provides support for a new modality of endocrine disruption via prostaglandin inhibition,” says senior study author Andreas Kortenkamp, a toxicologist at Brunel University in London. This study is thought to be the first to test pesticides for these effects.OPP is applied to citrus fruits and other crops after harvest to prevent spoilage. The general population is thought to consume levels of OPP well below recommended limits, although workers likely receive greater exposures.12 It is unknown whether OPP causes human health effects.© David Thurber/CorbisProstaglandins serve many purposes—from the promotion and resolution of the immune system’s inflammatory response7 to male sexual development in utero.5 Previous studies have suggested that synthesis of prostaglandin-D2 (PGD2) may serve as a back-up mechanism for androgen-driven differentiation of Sertoli cells8—testicular cells that play an important role in the development and production of sperm.A variety of mild analgesics (including acetaminophen, aspirin, and ibuprofen) have been shown to suppress PGD2 synthesis in human and rodent cell lines.9 In one study, self-reported use of aspirin, acetaminophen, or ibuprofen during pregnancy was associated with cryptorchidism in some boys but not others, and experimental findings for rats indicated shorter anogenital distance with exposure to acetaminophen or aspirin.10 According to the American Academy of Family Physicians, acetaminophen is generally considered safe for use during pregnancy, but this assessment is based on limited evidence.11 Pregnant women are advised to use aspirin and ibuprofen only under a doctor’s supervision.11In the current study, Kortenkamp and colleagues tested the ability of 24 pesticides commonly used in the European Union to suppress PGD2 synthesis in juvenile mouse Sertoli cells. Fifteen of the pesticides, including imidacloprid, cypermethrin, and ortho-phenylphenol (OPP), inhibited PGD2 synthesis in a concentration-dependent manner.6OPP, an antimicrobial agent used as a fungicide and sanitizer, was the most potent pesticide tested, suppressing PGD2 synthesis at a concentration of 175 nM. This made it nearly as potent as ibuprofen (used as a positive control), which suppressed PGD2 synthesis at a concentration of 128 nM.6 “We were really surprised by the potency of some of these pesticides, namely OPP,” Kortenkamp says.Molecular modeling suggested that OPP and other pesticides may interfere with prostaglandins by inhibiting cyclooxygenase-1 and cyclooxygenase-2—the enzymes responsible for prostaglandin synthesis—in a manner similar to ibuprofen. Eleven of the 15 pesticides shown to suppress prostaglandin synthesis also acted as antiandrogens, chemicals that interfere with androgen production by blocking the androgen receptor.6The new paper is important, because it shows that several of the investigated pesticides may obstruct both the androgen and prostaglandin signaling pathways, says David Kristensen, a toxicologist at the University of Copenhagen in Denmark. “The implications of this collective dual-hit scenario are not yet clear,” says Kristensen, who was not involved in the current study.It’s difficult to predict likely effects of these pesticides on humans from cell culture studies alone, Kortenkamp says. The next step for his team is to identify priority chemicals for testing in animal models. Factors such as the rate at which a chemical enters the body and how rapidly it is metabolized and excreted can help to predict chemicals that would be expected to show activity in fetal tissue at experimental doses.References1 Sharpe RMPathways of endocrine disruption during male sexual differentiation and masculinization.Best Pract Res Clin Endocrinol Metab 20(1):91-1102006., doi:10.1016/j.beem.2005.09.00516522522. Crossref, Medline, Google Scholar2 Christiansen Set al.Mixtures of endocrine disrupting contaminants modelled on human high end exposures: an exploratory study in rats.Int J Androl 35(3):303-3162012., doi:10.1111/j.1365-2605.2011.01242.x22372636. Crossref, Medline, Google Scholar3 Gupta C, Goldman ASThe arachidonic acid cascade is involved in the masculinizing action of testosterone on embryonic external genitalia in mice.Proc Natl Acad Sci USA. 83(12):4346-43491986., PMID:3086881. Crossref, Medline, Google Scholar4 Adams IR, McLaren ASexually dimorphic development of mouse primordial germ cells: switching from oogenesis to spermatogenesis.Development 129(5):1155-11642002., PMID:11874911. Medline, Google Scholar5 Wilhelm Det al.SOX9 regulates prostaglandin D synthase gene transcription in vivo to ensure testis development.J Biol Chem 282(14):10553-105602007., doi:10.1074/jbc.M60957820017277314. Crossref, Medline, Google Scholar6 Kugathas Set al.Effects of common pesticides on prostaglandin D2 (PGD2) inhibition in SC5 mouse Sertoli cells, evidence of binding at the COX2 active site, and implications for endocrine disruption.Environ Health Perspect 124(3):452-4592016., doi:10.1289/ehp.140954426359731. Link, Google Scholar7 Ricciotti E, FitzGerald GAProstaglandins and inflammation.Arterioscler Thromb Vasc Biol 31(5):986-10002011., doi:10.1161/ATVBAHA.110.20744921508345. Crossref, Medline, Google Scholar8 Koopman PThe delicate balance between male and female sex determining pathways: potential for disruption of early steps in sexual development.Int J Androl 33(2):252-2582010., doi:10.1111/j.1365-2605.2009.01001.x19845801. Crossref, Medline, Google Scholar9 Kristensen DMet al.Many putative endocrine disruptors inhibit prostaglandin synthesis.Environ Health Perspect 119(4):534-5412011., doi:10.1289/ehp.100263521081300. Link, Google Scholar10 Kristensen DMet al.Intrauterine exposure to mild analgesics is a risk factor for development of male reproductive disorders in human and rat.Human Reprod 26(1):235-2442011., doi:10.1093/humanrep/deq323. Crossref, Medline, Google Scholar11 Servey J, Chang JOver-the-counter medications in pregnancy.Am Fam Physician 90(8):548-5552014., PMID:25369643. Medline, Google Scholar12 CDC. Biomonitoring Summary: ortho-Phenylphenol [website]. Atlanta, GA:U.S. Centers for Disease Control and Prevention (updated 4 December 2013). Available: http://www.cdc.gov/biomonitoring/Orthophenylphenol_BiomonitoringSummary.html [accessed 16 March 2016]. Google ScholarFiguresReferencesRelatedDetailsCited by Zhao G, Li J, Yang F, Yin X, Ren F, Fang B and Pang G (2021) Spermiogenesis toxicity of imidacloprid in rats, possible role of CYP3A4, Chemosphere, 10.1016/j.chemosphere.2021.131120, 282, (131120), Online publication date: 1-Nov-2021. Related articlesEffects of Common Pesticides on Prostaglandin D2 (PGD2) Inhibition in SC5 Mouse Sertoli Cells, Evidence of Binding at the COX-2 Active Site, and Implications for Endocrine Disruption11 September 2015Environmental Health Perspectives Vol. 124, No. 4 April 2016Metrics About Article Metrics Publication History Originally published1 April 2016Published in print1 April 2016 Financial disclosuresPDF download License information EHP is an open-access journal published with support from the National Institute of Environmental Health Sciences, National Institutes of Health. All content is public domain unless otherwise noted. Note to readers with disabilities EHP strives to ensure that all journal content is accessible to all readers. However, some figures and Supplemental Material published in EHP articles may not conform to 508 standards due to the complexity of the information being presented. If you need assistance accessing journal content, please contact [email protected]. Our staff will work with you to assess and meet your accessibility needs within 3 working days." @default.
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