Endocrine disruption and reproduction impairment in zebrafish after long-term exposure to DE-71

2014 ◽  
Vol 33 (6) ◽  
pp. 1354-1362 ◽  
Author(s):  
Liqin Yu ◽  
Chunsheng Liu ◽  
Qi Chen ◽  
Bingsheng Zhou
Keyword(s):  
2021 ◽  
Vol 92 (8) ◽  
pp. A11.2-A11
Author(s):  
Ewelina de Leon ◽  
Graeme Yorston

Objectives/AimsTraumatic brain injury is a common cause of permanent or long-term disability,1 and up to 80% of people with moderate to severe brain injury have some degree of pituitary insufficiency. Endocrine disruption has been documented in medical literature since the 1940s,2-4 where central diabetes insipidus has been described as a common transient complication which causes polydipsia (insatiable thirst). However, polydipsia can be caused by other conditions. It is classified into dipsogenic, in a syndrome of disordered thirst-regulating mechanism in patients without psychiatric disease called dipsogenic diabetes insipidus, psychogenic, as a compulsive water drinking in patients with psychiatric conditions referred to as psychogenic polydipsia or psychogenic diabetes insipidus and iatrogenic where large quantities of water are consumed for health benefits. All of which are referred to as primary polydipsia if these conditions cannot be distinguished. Dipsogenic diabetes insipidus and psychogenic polydipsia can be easily mixed up, misdiagnosed or even unrecognised, mainly because their pathophysiology is still unclear. Are these conditions different, or is there anything that can relate them to each other? With this literature review, we are aiming to find the link between subsets of polydipsia after brain trauma, to compare proposed differential diagnosis and their functionality in clinical settings.MethodA literature review was conducted following a search of MEDLINE, CINAHL Plus, APA PsycArticles, APA PsycBooks, APA PsycInfo databases from 1858 onwards.ResultsWe will present our findings from the literature review.ConclusionPolydipsia is a common clinical problem and requires careful evaluation and management to prevent long term neurological sequelae, and there are no evidence-based treatment guidelines.References National Institute of Health and Care Excellence (NICE). (2019). Head Injury. CG176. Retrieved from: https://www.nice.org.uk/guidance/cg176 Escamilla RF, Lisser H. Simmonds disease: A clinical study with revie of the literature; Differentiation from anorexia nervosa by statistical analysis of 595 cases, 101 of which were provided pathologically. The Journal of Clinical Endocrinology & Metabolism 1942;2(2):6596. Porter RJ, Miller RA. Diabetes insipidus following closed head injury. Journal of Neurology, Neurosurgery, and Psychiatry 1946;11:528562. Webb NE, Little B, Loupee-Wilson S, Power EM. Traumatic brain injury and neuro-endocrine disruption: medical and psychosocial rehabilitation. NeuroRehabilitation (Reading, Mass.) 2014;34(4):625636.


2012 ◽  
Vol 12 (6) ◽  
pp. 837-843 ◽  
Author(s):  
Prince Nfodzo ◽  
Qinhong Hu ◽  
Hyeok Choi

The presence of triclosan (TCS) in water resources has drawn significant attention due to its endocrine disruption potential. Sulfate radicals (SRs), generated particularly by the metal-mediated activation of peroxymonosulfate (PMS), have been proposed to effectively decompose TCS and many other pharmaceuticals and personal care products. In spite of its significance for understanding the efficiency of SR generation and catalytic/non-catalytic nature of the oxidation reaction, metal speciation has not been adequately highlighted in previous studies. This study investigated the detailed changes in metal speciation in cobalt/PMS and iron/PMS systems and correlated it with TCS decomposition under different pH conditions. A rapid oxidation of Co2+ to Co3+ and Fe2+ to Fe3+ generally corresponded with pseudo-steady state decomposition kinetics of TCS after its initial fast decomposition. The presence of potential threshold concentrations of metals to effectively activate PMS was found. A strong catalytic activity was observed for Co/PMS system at pH 3, where most of Co was present in the form of dissolved Co2+. The pH impacts were different for Co/PMS and Fe/PMS. TCS oxidation was fast at pH 5 for Co and pH 3 for Fe. However, long-term mineralization of TCS seemed less dependent on pH.


2019 ◽  
Author(s):  
Clarissa Wormsbaecher ◽  
Andrea R. Hindman ◽  
Alex Avendano ◽  
Marcos Cortes ◽  
Andrew Bushman ◽  
...  

AbstractIn utero endocrine disruption is linked to increased risk of breast cancer later in life. Despite numerous studies establishing this linkage, the long-term molecular changes that predispose mammary cells to carcinogenic transformation are unknown. Several lines of evidence indicate the stroma mediates endocrine disruption following early-life (or in utero) exposure. Herein, we utilized BPA as a model of estrogenic endocrine disruption to analyze the long-term consequences in the stroma. Using RNA-seq transcriptional profiling of adult primary fibroblasts isolated from female mice exposed to BPA in utero, we identified deregulated genes associated with the extracellular matrix. Specifically, multiple collagen genes had increased expression in exposed mice. In line with the transcriptional data, collagen deposition is increased in adult BPA-exposed mice. We further demonstrate in vitro that fibroblasts exposed to BPA in utero remodel a collagen matrix, thereby decreasing permeability of the collagen matrix. These alterations to the mammary gland resulted in increased gland stiffness in the adult mice. Our data connects early life endocrine disruption to breast density. Interestingly, increased collagen deposition and gland stiffness were not observed in the developing glands of younger mice, suggesting risk factors for breast cancer continue to develop throughout life following these exposures. Finally, we assessed whether in utero exposure to two other endocrine disruptors, BPS and DES, also increase breast stiffness in adult mice. While DES increased breast stiffness, BPS did not, suggesting this BPA alternative may in fact pose less breast cancer risk than its predecessor. As breast stiffness, extracellular matrix density, and collagen deposition have been directly linked to breast cancer risk, these data mechanistically link endocrine disruptor exposures and molecular alterations to increased disease susceptibility in the gland.


Author(s):  
W. J. Langston

AbstractContaminants causing sex-altering, endocrine disrupting-like (ED) effects, or otherwise influencing reproduction, have been of growing concern to humans for more than 50 years. They have also been a perturbing, though less well-studied, phenomenon in marine organisms, following the recognition of tributyltin (TBT)-induced imposex and population extinctions in (neo)gastropods in the 1970s. Whilst ED impacts in mammals and fish are characterized by mimicry or antagonism of endogenous hormones by environmental contaminants (acting through Nuclear Receptors which are present in all metazoans) much less is known regarding pathways to effects in invertebrates. Despite the absence of a defined steroidal/mechanistic component, the extent, severity and widespread nature of ED-like manifestations and altered sexual characteristics observed in marine invertebrates gives rise to comparable concerns, and have been a long-term component of the MBA's research remit. The manifestations seen in sensitive taxa such as molluscs and crustaceans confirm they are valuable indicators of environmental quality, and should be exploited in this capacity whilst we seek to understand the pervasiveness and underlying mechanisms. In so doing, invertebrate indicators address aims of organizations, such as the EEA, OECD, UNEP and WHO, charged with management and monitoring of chemicals and ensuring that adverse effects on humans and the environment are minimized (Bergman et al., 2013). In view of the recent general declines in marine biodiversity, and the potential contribution of ED-like phenomena, safeguarding against deleterious effects through increased research which links pollutant exposure with reproductive dysfunction among invertebrates, is seen as a high priority.


2002 ◽  
Vol 18 (2) ◽  
pp. 495-504 ◽  
Author(s):  
Ellen K. Silbergeld ◽  
Jodi A. Flaws ◽  
Ken M. Brown

Endocrine disruption is a hypothesis of common mode of action that may define a set of structurally varied chemicals, both natural and synthetic. Their common mode of action may suggest that they produce or contribute to similar toxic effects, although this has been difficult to demonstrate. Insights from developmental biology suggest that development of hormone sensitive systems, such as the brain and the genitourinary tract, may be particularly sensitive to EDCs. Because these systems are both organized and later activated by hormones, the brain and vagina may be valuable model systems to study the toxicity of EDCs in females and to elucidate mechanisms whereby early exposures appear to affect long term function.


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