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Health Effects of Endocrine-Disrupting Chemicals on Wildlife, with Special Reference to the European Situation
TLDR
Many wildlife species may be exposed to biologically active concentrations of endocrine-disrupting chemicals, and although most observed effects currently reported concern heavily polluted areas, endocrine disruption is a potential global problem.
The avian egg as a test system for endocrine disrupters: effects of diethylstilbestrol and ethynylestradiol on sex organ development.
TLDR
Feminization of the left testis in males proved to be the most sensitive endpoint for estrogenic activity of xenobiotics in Japanese quail embryos, and the quail egg is proposed as a simple in vivo test system for estrogenIC compounds.
Identification of hydroxylated polybrominated diphenyl ether metabolites in blood plasma from polybrominated diphenyl ether exposed rats.
TLDR
The results show that OH-PBDE congeners have an ability to be retained in rat blood, most likely by a mechanism similar to that of OH-PCBs, which will be useful for determination of the origin of PBDEs present in wildlife and in humans.
The Impact of Endocrine Disruption: A Consensus Statement on the State of the Science
TLDR
The basis for these key concerns is described in the State of the Science of Endocrine Disrupting Chemicals - 2012, that includes scientific information on human and Wildlife impacts and lists key concerns for decision makers and others concerned about the future of human and wildlife health.
Cytochrome P4501A induction in rainbow trout gills and liver following exposure to waterborne indigo, benzo[a]pyrene and 3,3',4,4',5-pentachlorobiphenyl.
TLDR
The observation that the low BaP and indigo concentrations induced EROD activity markedly in the gills but only slightly or not at all in the liver, supports the contention that readily metabolized AhR agonists may escape detection when hepatic EROD activities is used for environmental monitoring.
Irreversible binding and toxicity of the herbicide dichlobenil (2,6-dichlorobenzonitrile) in the olfactory mucosa of mice.
TLDR
It is proposed that dichlobenil induces a primary lesion in the glands of Bowman, resulting from the pronounced binding of a metabolite in these glands, and the toxicity to the olfactory neuroepithelium may be secondary to the destruction of the glands in Bowman.
Controlling persistent organic pollutants-what next?
TLDR
A tiered approach is proposed for screening the large number of untested chemical substances according to their long-range transport potential, persistence and bioaccumulative potential prior to more detailed risk assessments.
Metabolic activation and toxicity of a DDT-metabolite, 3-methylsulphonyl-DDE, in the adrenal zona fasciculata in mice.
TLDR
3-MeSO2-DDE is a persistent environmental pollutant with a unique ability to produce acute toxicity subsequent to metabolic activation in a mammalian tissue and to cause acute toxicity after single doses down to 25 mg/kg.
Embryonic exposure to o,p'-DDT causes eggshell thinning and altered shell gland carbonic anhydrase expression in the domestic hen.
TLDR
The hypothesis that eggshell thinning in avian wildlife can result from a functional malformation in the shell gland, induced by embryonic exposure to estrogenic substances is supported.
Cytochrome P450-catalyzed binding of 3-methylsulfonyl-DDE and o,p'-DDD in human adrenal zona fasciculata/reticularis.
TLDR
It is suggested that MeSO(2)-DDE might act as a potent adrenocorticolytic agent in humans following a local CYP11B1-catalyzed activation to a reactive intermediate in mice.
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