Embryos as targets of endocrine disrupting contaminants in wildlife

Abstract

Environmental contaminants are now a ubiquitous part of the ecological landscape, and a growing literature describes the ability of many of these chemicals to alter the developmental trajectory of the embryo. Because many environmental pollutants readily bioaccumulate in lipid rich tissues, wildlife can attain considerable body burdens. Embryos are often exposed to these pollutants through maternal transfer, and a growing number of studies report long-term or permanent developmental consequences. Many biological mechanisms are reportedly affected by environmental contaminants in the developing embryo and fetus, including neurodevelopment, steroidogenesis, gonadal differentiation, and liver function. Embryos are not exposed to one chemical at a time, but are chronically exposed to many chemicals simultaneously. Mixture studies show that for some developmental disorders, mixtures of chemicals cause a more deleterious response than would be predicted from their individual toxicities. Synergistic responses to low dose mixtures make it difficult to estimate developmental outcomes, and as such, traditional toxicity testing often results in an underestimate of exposure risks. In addition, the knowledge that biological systems do not necessarily respond in a dose-dependent fashion, and that very low doses of a chemical can prove more harmful than higher doses, has created a paradigm shift in studies of environmental contaminant-induced dysfunction. Although laboratory studies are critical for providing dose-response relationships and determining specific mechanisms involved in disease etiology, wildlife sentinels more accurately reflect the genetic diversity of real world exposure conditions, and continue to alert scientists and health professionals alike of the consequences of developmental exposures to environmental pollutants.

Anaerobic degradation of Polychlorinated Biphenyls (PCBs) and Polychlorinated Biphenyls Ethers (PBDEs), and microbial community dynamics of electronic waste-contaminated soil

“…Extremely high levels of PCBs and PBDEs are found in soil, water, air, sediment, and vegetation on/around e-waste recycling sites (Wong et al, 2007). PCBs and PBDEs are persistent, bioaccumulative and toxic, disrupting endocrine systems and posing serious threats to local ecosystems and human health (Egloff et al, 2011;Frye et al, 2012;Hamlin and Guillette, 2011;Purser, 2001;She et al, 2013;Wang et al, 2010;Zhou et al, 2001).…”

Gonadal Differentiation in Reptiles Exhibiting Environmental Sex Determination

“…It became rapidly clear that studies of wildlife -especially studies examining the gonadal development and differentiation in wildlife -would be critical for an understanding of the role of EDCs in wild populations. Studies of reptilian sex determination and gonadal differentiation have been central to discussions of environmental health and risk [Iguchi et al, 2001;Hamlin and Guillette, 2011]. Our group has hypothesized that embryonic exposure to contaminants capable of acting as endocrine disruptors could induce permanent organizational -epigenetic -changes in the developing organism [Guillette and Moore, 2006;Guillette and Iguchi, 2012].…”

“…Both sex determination systems can be 'overridden' by exposure of the developing embryo to sex steroid hormone exposures or chemicals with these properties. Thus, reptiles are sensitive to environmental factors, such as climate change and exposure to endocrine disrupting compounds [Hamlin and Guillette, 2011]. Indeed, in ovo exposure studies have demonstrated that sex ratios of American alligators (Alligator mississippiensis) [Milnes et al, 2005] and redeared sliders (Trachemys scripta) [Willingham and Crews, 1999] are sensitive to environmental contaminants with endocrine disrupting activity (EDCs).…”

Endocrine disrupting chemicals

“…The hypothalamic kisspeptin-1 (KiSS-1) and its G protein-coupled receptor (GPR54) act as the gatekeeper to control the secretion of gonadotrophin releasing hormone (GnRH), which regulates the anterior pituitary hormones-luteinizing hormone (LH) and follicle stimulating hormone (FSH), and testicular hormones-testosterone, activin and inhibin B. 41,68,70,71 Since neuroendocrine actions of EDCs have been shown, [72][73][74] HPG circuitry signaling can be the EDC target during perinatal development. Any interruption on the hypothalamic circuitry, hormonal mediated regulation or on the constituents at the microenvironments in seminiferous tubules may result in a transient/long-term modification of the hormonal feedback circuitry, leading to the disturbance of spermatogenesis.…”