| Endocrine Disrupting Contaminants--Beyond the Dogma Louis J. Guillette Jr. Department of Zoology, University of Florida, Gainesville, Florida, USA Abstract
Descriptions of endocrine disruption have largely been associated with wildlife and driven by observations documenting estrogenic, androgenic, antiandrogenic, and antithyroid actions. These actions, in response to exposure to ecologically relevant concentrations of various environmental contaminants, have now been established in numerous vertebrate species. However, many potential mechanisms and endocrine actions have not been studied. For example, the DDT [1,1,1-trichloro-2,2-bis(p-chlorophenyl) ethane] metabolite, p,pī-DDE [1,1-dichloro-2,2-bis(p-chlorophenyl) ethylene] is known to disrupt prostaglandin synthesis in the uterus of birds, providing part of the explanation for DDT-induced egg shell thinning. Few studies have examined prostaglandin synthesis as a target for endocrine disruption, yet these hormones are active in reproduction, immune responses, and cardiovascular physiology. Future studies must broaden the basic science approach to endocrine disruption, thereby expanding the mechanisms and endocrine end points examined. This goal should be accomplished even if the primary influence and funding continue to emphasize a narrower approach based on regulatory needs. Without this broader approach, research into endocrine disruption will become dominated by a narrow dogma, focusing on a few end points and mechanisms. Key words: adrenal steroidogenesis, endocrine disruption, estrogens, hormone metabolism, nitrate, progesterone, prostaglandins. Environ Health Perspect 114(suppl 1) :9-12 (2006) . http: //dx.doi.org/ doi:10.1289/ehp.8045 available via http://dx.doi.org/ [Online 21 October 2005]
This article is part of the monograph "The Ecological Relevance of Chemically Induced Endocrine Disruption in Wildlife." Address correspondence to L.J. Guillette Jr., Department of Zoology, 223 Bartram Hall - Box 118525, University of Florida, Gainesville, FL 32611 USA. Telephone: 352-392-1098. Fax: 352-392-3704. E-mail: ljg@zoo.ufl.edu I thank T. Iguchi, J. McLachlan, E. Orlando, D. Pickford, and my graduate students T. Edwards, B. Moore, M. Milnes, and M. Gunderson for stimulating discussions that led to this commentary. The research described from my laboratory was supported by grants from the U.S. Environmental Protection Agency, the National Institute of Environmental Health Sciences, and the Marisla Foundation The authors declare they have no competing financial interests. Received 31 January 2005 ; accepted 22 August 2005.
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