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Development problems induced by endocrine disruptors (EDCs) are currently understudied. However, early exposure to EDCs may lead to deleterious and permanent problems in later lifetime. Zebrafish (Danio rerio) transgenic lines with tissue-specific expression of GFP are useful tools to identify the organs affected by a given compound. We have used 7 transgenic lines to visualize in vivo whether 6 known EDCs and 3 other pharmaceuticals can alter organogenesis during development of zebrafish. This screen revealed that 4 chemicals have effects on 4 different organs. The EDC tetrabromobisphenol-A, as well as the tested medicines (diclofenac, trichostatin A and valproic acid) disrupt vascular system development in zebrafish embryo. Moreover, HDAC inhibitors trichostatin A and valproic acid inhibit both endocrine and exocrine pancreas development. Developmental delays were also induced by trichostatin A and valproic acid in the liver and in the pharyngeal teeth. Traditional Chinese medicines (TCMs) are important components of modern medicine. However we know little about the biological activities of TCMs compounds during development. We used zebrafish embryos to study the effects of 3 plants and 5 of their major compounds on the development. We observed that zebrafish embryogenesis was delayed by water extracts from Astragalus membranaceus and Akebia quinata. We also found that the vascular development was affected at different levels by Salvia miltiorrhiza water extracts and by its 3 major components either used alone or mixed together.Our results show that EDCs and TCMs can cause problems during zebrafish embryogenesis. They also show that zebrafish is a powerful tool for rapid in vivo screening of small molecules and their effects on development. This work also enables us to draw a parallel between EDC and some TCMS, which may act on similar targets, such as nuclear receptors.
Environmental pollutants are suspected of causing observed adverse effects on development and reproduction in fish and wildlife. Evidence from the laboratory and field suggests that low levels of synthetic or natural chemicals that modulate or disrupt endocrine processes may be responsible. The aquatic environment is a sink for most all potential endocrine disrupting chemicals (EDCs). From egg fertilization to spawning, fish may be exposed to complex mixtures of steroidogenic chemicals that can interfere with the important activational and organizational processes of their endogenous hormones. One consequence of exposure to EDCs may be disruption of the normal mechanisms of sexual development and differentiation, processes that are highly hormone dependent, with subsequent adverse effects on reproduction. My experiments address the hypothesis that exposure to EDCs during early ontogeny affects sexual development and differentiation in fish manifest at maturation. The dr-R strain of medaka was used as the test organism because of qualities that make it a good laboratory animal model and because it possesses a sex-linked gene for body color allowing visual determination of genetic sex from hatch. Medaka were exposed in ovo by nano-injection to five chemical compounds known or suspected to be hormone mimics or disruptors. Details of the effects resulting from exposure to the synthetic sex steroids ethinyl estradiol (EE 2) and methyl testosterone (MT) provided a reference and established a model for predicting effects of in ovo exposure to chemicals which mimic estrogens and androgens. Effects on medaka exposed to the EDCs, o, p ' -DDE and 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), and three mixtures of polychlorinated naphthalenes (PCN), which have not been tested for their endocrine disrupting potential, were also investigated. In ovo exposure to 0.5 and 2.5 ng EE 2 /embryo or 0.8 and 8.0 ng MT/embryo affected sexual differentiation by causing sex reversal in males and females, respectively. Sexual development of male and female gonads was also affected at these doses. Most notably, all doses of MT resulted in precocious maturation of male and female medaka. Effects on sexual differentiation of the gonads were not as apparent for o, p ' -DDE, TCDD, and the PCNs as were effects on sexual development. Observed effects of these chemicals included one or more abnormalities: histopathological lesions (e.g., atresia), reduced gonad size, and changes in primary germ cell numbers along with volume of primordial gonads. Results for these chemicals together with other's field and laboratory observations provide further evidence that environmental EDCs may be adversely affecting reproduction and development of wild fishes. These results also support the utility of laboratory studies with the dr-R medaka model within the framework of a weight-of-evidence approach to establish a cause-and-effect relationship between environmental exposure to EDCs and reproductive impairment at the individual and population levels.
Endocrine-disrupting chemicals (EDCs), including polychlorinated biphenyls (PCBs), bisphenol A (BPA), pharmaceutical drugs, and pesticides, affect a variety of hormone-regulated physiological pathways in humans and wildlife. The occurrence of these EDCs in the aquatic environment is linked with vertebrates,Äô health alteration. EDCs exhibit lipophilic characteristics and bind to hydrophobic areas of steroid receptors, such as the estrogen receptor, which are involved in vertebrate developmental regulation. Mainly, EDCs modify the transcription of several genes involved in individual homeostasis. Zebrafish conserve many developmental pathways found in humans, which makes it an appreciated model system for EDCs research studies, especially on early organ development. In the current chapter, we emphasize on latest published papers of EDCs effects on lateral line regeneration in zebrafish larvae. Similarly, we describe other special impacts of EDCs exposure. In conclusion, we make the case that the zebrafish lateral line exposed to EDCs can provide important insights into human health.
The field of endocrine disruption has been the focus of increasing attention from scientists and the general public in the past 30 years, amidst concerns that exposure to environmental chemicals with the potential to alter endocrine system function, known as endocrine disrupting chemicals (EDCs), may be contributing to an overall decline in wildlife populations and the reproductive health of humans. These concerns are based on observations of adverse effects of EDCs on marine and land animals, an increased incidence of reproductive and endocrine disease in humans, epidemiological evidence for links between body burden and disease, and endocrine disruption in laboratory animals following exposure to EDCs. Owing to its role in regulation of endocrine function as well as its responsiveness to hormones, the developing brain is an especially vulnerable target for many classes of EDCs. This book will address the evidence for EDC action on the developing brain, organized into 7 chapters. Topics covered include background about EDCs, evidence for exposures, concerns about EDC effects in the developing organism, and particularly on the developing nervous system, how EDCs perturb the brain's neuroendocrine systems, transgenerational epigenetic effects of EDCs, EDC effects on non-reproductive behaviors, and future perspectives. This is the first book completely dedicated to understanding links between EDCs and the developing brain, an area of emerging importance for human health.
This book addresses the biological effects of the reasonably large number of classes of compounds that have been recognized as endocrine disrupters. These compounds have been found to persist as pollutants in the environment, and have been blamed for causing developmental disorders and/or fertility problems in fish, amphibians, reptiles, birds, and possibly humans. This book presents the relevant fundamentals of the endocrine systems of animals and humans, the toxicology, developmental toxicology, ecology, and risk assessment methods, and lays out the current state of understanding for the whole field, organized by the classes of compounds that have been identified as endocrine disrupters.