The effects of UV-B radiation and endocrine-disrupting chemicals (EDCs) on the biology of amphibians

2001 ◽  
Vol 9 (2) ◽  
pp. 61-80 ◽  
Author(s):  
D Crump

Statistical meta-analysis of large and diverse data sets has indicated that amphibians have been declining worldwide since the 1960s. Exposure to UV-B radiation (280–320 nm) and endocrine-disrupting chemicals (EDCs) have been considered as possible hypotheses to explain the observed declines. Equivocal conclusions have been reached with respect to the effects of UV-B on amphibian populations. Field and laboratory studies employing both ecologically relevant and enhanced UV-B levels have been conducted using a variety of amphibian species and reports differ with respect to the most sensitive developmental stage and the ultimate implications. UV-B radiation has also been shown to interact with other stressors (e.g., pesticides, polycyclic aromatic hydrocarbons, low pH) resulting in decreased survivorship for several amphibian species. Limited evidence of reproductive toxicity of xenobiotics in amphibians exist; however, early exposure to EDCs could cause abnormal development of the amphibian reproductive system, inhibit vital hormone messages that drive metamorphosis, and ultimately contribute to the decline of some amphibian populations. The available evidence suggests that more than one agent is contributing to amphibian population declines and the following review narrows the focus to address the existing data on the effects of UV-B, alone and in combination with other stressors, and EDCs on amphibian survivorship and development. Key words: amphibians, UV-B radiation, endocrine-disrupting chemicals, declines, review.

Author(s):  
Jane A. Plant ◽  
Devra L. Davis

Cancers of the breast and prostate, which together with those of the ovaries, endometrium and testes are hormone-dependent, are among the most common forms of cancers affecting women and men respectively throughout the developed world (IARC VII 1997, Miller and Sharp 1998). The incidence of breast, prostate, and testicular cancers has risen dramatically in most European and North American countries and in Japan and Australasia since cancer registries were first compiled in the 1960s (WHO/IARC Web site). For instance, women and men born in Generation X in the U.S. and Europe today have twice the risk of developing breast and prostate cancer than their grandparents faced (Dinse et al. 1999). Several lines of evidence indicate that environmental factors, broadly conceived, may account for some of the recent changes in patterns of hormonally dependent cancers. Although rates are about 4 times lower in Asian countries than in European ones, they are increasing most rapidly in the former (Hoel et al. 1992). People who migrate tend to develop the cancer rate of their new countries. Studies of highly exposed workers consistently find that those working with certain plastics, organic solvents, pesticides, and other toxic chemicals tend to have higher risks of several hormonally dependent cancers (Davis and Muir 1995). Dietary factors can be involved in these patterns in two ways. Food constituents, such as dairy and animal protein products, can affect hormonal metabolism directly. In addition, foods can contain contaminants such as growth stimulating substances, pesticides, and packaging materials that can function as endocrine disrupting chemicals (EDCs). In the past decade, a number of major national and international reports have noted the possible role of EDCs for hormone-related illnesses including breast and prostate cancer, including the Weybridge report of the European Environment Agency of 1996 (EUR 17549 1997) and the Royal Society Report on Endocrine Disrupting Chemicals (Royal Soc. 2000). This chapter presents some recent information on the sources of EDCs in the environment, outlines mechanisms by which these materials can increase the risk of hormonally dependent cancers, and discusses insights from geochemistry that may be pertinent to this work.


2016 ◽  
Vol 124 (11) ◽  
pp. 1785-1793 ◽  
Author(s):  
Laura Birks ◽  
Maribel Casas ◽  
Ana M. Garcia ◽  
Jan Alexander ◽  
Henrique Barros ◽  
...  

Reproduction ◽  
2011 ◽  
Vol 142 (5) ◽  
pp. 633-646 ◽  
Author(s):  
Zelieann R Craig ◽  
Wei Wang ◽  
Jodi A Flaws

Endocrine-disrupting chemicals (EDCs) are exogenous agents with the ability to interfere with processes regulated by endogenous hormones. One such process is female reproductive function. The major reproductive organ in the female is the ovary. Disruptions in ovarian processes by EDCs can lead to adverse outcomes such as anovulation, infertility, estrogen deficiency, and premature ovarian failure among others. This review summarizes the effects of EDCs on ovarian function by describing how they interfere with hormone signaling via two mechanisms: altering the availability of ovarian hormones, and altering binding and activity of the hormone at the receptor level. Among the chemicals covered are pesticides (e.g. dichlorodiphenyltrichloroethane and methoxychlor), plasticizers (e.g. bisphenol A and phthalates), dioxins, polychlorinated biphenyls, and polycyclic aromatic hydrocarbons (e.g. benzo[a]pyrene).


Author(s):  
Sir Peter Gluckman ◽  
Mark Hanson ◽  
Chong Yap Seng ◽  
Anne Bardsley

Advice for pregnant women on food avoidance, dangerous exposures, and inappropriate behaviours abounds on the internet and through various information sources. This chapter reviews the evidence base for such advice and clarifies issues where common advice is not supported by credible data. Foods containing potential teratogens, mutagens, or toxicants that need consideration include liver (high vitamin A), some herbal teas, contaminated grains, predatory fish, caffeine-containing foods, and various sources of foodborne infections. Exposure to environmental toxicants such as lead, pesticides, herbicides, polycyclic aromatic hydrocarbons, bisphenol-A, and other endocrine-disrupting chemicals should be avoided, as should alcohol consumption and cigarette smoking. Restrictive diets and unusual dietary cravings (pica) need to be properly managed. Evidence for harm from personal care products is generally weak, but pregnant women may choose to avoid some unnecessary exposures.


Author(s):  
Elvira V Bräuner ◽  
Youn-Hee Lim ◽  
Trine Koch ◽  
Cecilie S Uldbjerg ◽  
Laura S Gregersen ◽  
...  

Abstract The incidence of many hormone-dependent diseases, including testicular cancer, have sharply increased in all high-income countries during the 20th century. This is not fully explained by established risk factors. Concurrent, increasing exposure to antiandrogenic environmental endocrine disrupting chemicals (EDCs) in fetal life may partially explain this trend. This systematic review assessed available evidence regarding the association between environmental EDC exposure and risk of testicular cancer (seminomas and non-seminomas). Following PRISMA guidelines, a search of English peer-reviewed literature published prior to December 14 th, 2020, in the databases PubMed and Embase® was performed. Among the 279 identified records, 19 were eligible for quality assessment and 10 for further meta-analysis. The completeness of reporting was high across papers, but over 50% were considered subject to potential risk of bias. Mean age at diagnosis was 31.9 years. None considered effects of EDCs multipollutant mixtures. The meta-analyses showed that maternal exposure to combined EDCs was associated with a higher risk of testicular cancer in male offspring (summary RRs: 2.16, (95% CI:1.78-2.62); 1.93 (95% CI:1.49-2.48); 2.78 (95% CI:2.27-3.41) for all, seminoma, non-seminoma respectively). Similarly, high maternal exposures to grouped organochlorines and organo-halogens were associated with higher risk of seminoma and non-seminoma in the offspring. Summary estimates related to postnatal adult male EDC exposures were inconsistent.Maternal but not postnatal adult male, EDC exposures were consistently associated with a higher risk of testicular cancer, particularly risk of non-seminomas. However, the quality of studies was mixed and considering the fields complexity, more prospective studies of prenatal EDC multipollutant mixture exposures and testicular cancer are needed.


Reproduction ◽  
2014 ◽  
Vol 147 (4) ◽  
pp. 489-501 ◽  
Author(s):  
Marta Axelstad ◽  
Sofie Christiansen ◽  
Julie Boberg ◽  
Martin Scholze ◽  
Pernille Rosenskjold Jacobsen ◽  
...  

Reproductive toxicity was investigated in rats after developmental exposure to a mixture of 13 endocrine-disrupting contaminants, including pesticides, plastic and cosmetic ingredients, and paracetamol. The mixture was composed on the basis of information about high-end human exposures, and the dose levels reflecting 100, 200, and 450 times this exposure were tested. The compounds were also grouped according to their estrogenicity or anti-androgenicity, and their joint effects were tested at two different doses, with each group reflecting 200 or 450 times human exposure. In addition, a single paracetamol dose was tested (350 mg/kg per day). All exposures and a vehicle were administered by oral gavage to time-mated Wistar dams rats throughout gestation and lactation, and their offspring were assessed for reproductive effects at birth and in prepuberty. The mixture doses, which included the anti-androgenic compounds, affected the male offspring by causing decreased anogenital distance, increased nipple retention (NR), and reduced ventral prostate weights, at both medium and high doses. In addition, the weights of the levator ani/bulbocavernosus muscle (LABC) were decreased at the high dose of anti-androgen mixture. No effects were seen after exposure to the estrogenic chemicals alone, whereas males exposed solely to paracetamol showed decreased LABC weights and increased NR. Thus adverse reproductive effects were observed at mixtures reflecting 200 times high-end human exposure, which is relatively close to the safety margin covered by the regulatory uncertainty factor of 100. This suggests that highly exposed human population groups may not be sufficiently protected against mixtures of endocrine-disrupting chemicals.


2015 ◽  
Vol 8 (4) ◽  
pp. 516-532 ◽  
Author(s):  
Yan Song ◽  
Elizabeth L. Chou ◽  
Aileen Baecker ◽  
Nai-Chieh Y. You ◽  
Yiqing Song ◽  
...  

2019 ◽  
Vol 20 (5) ◽  
pp. 1209 ◽  
Author(s):  
Jaeseong Jeong ◽  
Hunbeen Kim ◽  
Jinhee Choi

Molecular docking is used to analyze structural complexes of a target with its ligand for understanding the chemical and structural basis of target specificity. This method has the potential to be applied for discovering molecular initiating events (MIEs) in the Adverse Outcome Pathway framework. In this study, we aimed to develop in silico–in vivo combined approach as a tool for identifying potential MIEs. We used environmental chemicals from Tox21 database to identify potential endocrine-disrupting chemicals (EDCs) through molecular docking simulation, using estrogen receptor (ER), androgen receptor (AR) and their homology models in the nematode Caenorhabditis elegans (NHR-14 and NHR-69, respectively). In vivo validation was conducted on the selected EDCs with C. elegans reproductive toxicity assay using wildtype N2, nhr-14, and nhr-69 loss-of-function mutant strains. The chemicals showed high binding affinity to tested receptors and showed the high in vivo reproductive toxicity, and this was further confirmed using the mutant strains. The present study demonstrates that the binding affinity from the molecular docking potentially correlates with in vivo toxicity. These results prove that our in silico–in vivo combined approach has the potential to be applied for identifying MIEs. This study also suggests the potential of C. elegans as useful in the in vivo model for validating the in silico approach.


2020 ◽  
Vol 21 (23) ◽  
pp. 9191
Author(s):  
Elizabeth C. Plunk ◽  
Sean M. Richards

Anthropogenic endocrine-disrupting chemicals (EDCs) can contaminate air, soil, and water. Human exposures to EDCs occur through inhalation, absorption, and ingestion. EDCs act by disrupting various pathways in the endocrine system. When the hypothalamic–pituitary–gonadal (HPG) axis is disrupted by EDCs, there can be effects on fertility in both men and women. Not only can fertility be indirectly affected by EDC disruptions of the HPG axis, but EDCs can also directly affect the menstrual cycle and sperm morphology. In this review, we will discuss the current findings on EDCs that can be inhaled. This review examines effects of exposure to prominent EDCs: brominated and organophosphate flame retardants, diesel exhaust, polycyclic aromatic hydrocarbons, cadmium and lead, TCDD, and polychlorinated biphenyls on fertility through alterations that disrupt the HPG axis and fertility through inhalation. Although the studies included herein include multiple exposure routes, all the studies indicate receptor interactions that can occur from inhalation and the associated effects of all compounds on the HPG axis and subsequent fertility.


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