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Tests on Naturally Voided Body Fluids
Published in Robert B. Northrop, Non-Invasive Instrumentation and Measurement in Medical Diagnosis, 2017
Tests to determine the concentrations of certain hormones in the urine can also aid in the diagnosis of hormonal regulatory disorders. In Table 8.9derived from data in Collins (1968), we illustrate the diseases and conditions associated with unbalances of urine 17-hydroxycorticosteroids, 17-ketosteroids, aldosterone, and gonadotropins. At least 13 steroid hormones are made in the adrenal cortex; it is a busy place. The 17-hydroxycorticosteroids are produced from cholesterol in response to ACTH secreted by the anterior pituitary gland; they include the glucocorticoids hormones progesterone and cortisol. The 17-ketosteroids include the androgenic hormones dehydroepiandosterone (DEA), and testosterone (made in the testicles). The mineral corticoid, aldosterone, is also synthesized in the adrenal cortex (West 1985). Its principle role is in the regulation of plasma potassium ions (Northrop 2000). Human anterior pituitary gonadotropin hormones include the glycoproteins, follicle-stimulating hormone, and luteinizing hormone.
Xenobiotic metabolism and transport in Caenorhabditis elegans
Published in Journal of Toxicology and Environmental Health, Part B, 2021
Jessica H. Hartman, Samuel J. Widmayer, Christina M. Bergemann, Dillon E. King, Katherine S. Morton, Riccardo F. Romersi, Laura E. Jameson, Maxwell C. K. Leung, Erik C. Andersen, Stefan Taubert, Joel N. Meyer
Although vertebrate endocrine-related receptors are not generally thought of as major regulators of xenobiotic transport and metabolism, a digression on the potential for C. elegans to be used as a model organism for endocrine disruption is warranted. Endocrine disruptors are molecules that interfere with an organism’s intrinsic endocrine systems, which often act by targeting NHRs that regulate endogenous endocrine signals such as estrogen and mammalian NHR estrogen receptor. As such, endocrine disruptors have the potential to disturb the normal physiology and development of an organism. Endocrine disruption is a major concern in environmental toxicology with great relevance for human and wildlife health (Hotchkiss et al. 2008; National Academies of Sciences, Engineering, and Medicine 2017). There are some investigations reporting results of using C. elegans to study endocrine disruption, and clearly chemicals that are agonists of vertebrate endocrine receptors exert effects in C. elegans (Cao et al. 2020; Chen et al. 2019; Custodia et al. 2001; Fischer et al. 2012; Jeong, Kim, and Choi 2019; Mimoto et al. 2007). However, it needs to be emphasized that conclusions regarding the mechanism by which these effects are mediated be interpreted with great caution. It is far from clear that responses result from presumed receptor agonist or antagonist binding to a worm homolog of the vertebrate receptor. As noted above, sequence comparisons suggest that the NR1I group of classical detoxification NHRs is apparently absent in C. elegans. In addition, the families encoding the classical mammalian steroid/thyroid receptors: NR1A thyroid hormone receptors (TRs), NR3A estrogen receptors (ERs), and NR3C 3-ketosteroid receptors including glucocorticoid receptor (GR), mineralocorticoid receptor (MR), progesterone receptor (PR), and androgen receptor (AR) are also absent (Nuclear Receptors Nomenclature, Committee 1999; Taubert, Ward, and Yamamoto 2011; Weikum, Liu, and Ortlund 2018). Accordingly, to our knowledge, no broad evidence base supports the concept that any C. elegans NHR is (in)activated by (ant)agonists of any of these vertebrate NHR, which would render it and the nematode susceptible to endocrine disruption by the presumed pathway, such as by a xenoestrogens acting on a worm “estrogen receptor.” Therefore, although it is not impossible that functional homologs of vertebrate endocrine receptors exist, one can argue that the burden of proof is on demonstrating such functional homology, which needs to be tested rigorously. On the other hand, it is entirely possible that C. elegans may serve as a useful model for the influence of NHR-activating xenobiotics in invertebrates (Hoss and Weltje 2007). Although evidence for such events is currently also lacking, one cannot rule out that endocrine disruption of DAF-12 driven developmental pathways may occur.