Inhibition of Endogenous PSA Expression by DIM
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shared by Nathan Goodyear on 17 Jul 13
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Organophosphate Antagonism of the Androgen Receptor - 0 views
toxsci.oxfordjournals.org/...1.full
organophosphates insecticides xenoestrogen androgen receptor antagonists androgen receptor antagonist antagonists
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shared by Nathan Goodyear on 19 May 14
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Targeting estrogen receptor subtypes (ERα and ERβ) with selective ER modulato... - 0 views
joe.endocrinology-journals.org/...325.abstract
ovarian cancer ER alpha ER beta ER-alpha ER-beta ovary estrogen receptor receptors ER
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Studies in breast cancer and prostate cancer have revealed different effects by ER alpha vs ER beta. It is no surprise that the same effects are found in ovarian cancer. This study found ER alpha antagonists and ER beta agonists "significantly" suppressed growth in the ovarian cancer cell lines SKOV3 and OV2008. Also, ER alpha agonist and ER beta antagonist "significantly" increased growth in the same cell lines. These findings point to in increased proliferation with ER alpha and decreased with ER beta. This is consistent with breast and prostate cancer also.
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shared by Nathan Goodyear on 05 Nov 14
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Plant-derived 3,3′-Diindolylmethane Is a Strong Androgen Antagonist in Human ... - 0 views
www.jbc.org/...21136.full
DIM I3C PSA AR androgen receptor prostate cancer men male hormone hormones androgen
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DIM has a strong affinity for both the mutant AR inLNCaP cells and for recombinant wild-type human AR
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PSA has been reported to promote the proliferation, migration, and metastasis of prostate cancer cells through several mechanisms, including cleavage of insulin-like growth factor-binding protein-3 and degradation of extracellular matrix proteins fibronectin and laminin
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down-regulation of PSA expression may be important in the antiproliferative effects of DIM in LNCaP cells
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Dexamethasone prevents postoperative nausea and vomiting: Benefit versus risk - Science... - 0 views
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Dexamethasone is a synthetic form of adrenocorticoid, and acts mainly as a glucocorticoid receptor with almost no mineralocorticoid receptor functions
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serotonin Type 3 receptor antagonist (ondansetron, dolasetron, and granisetron), dopamine Type 2 receptor antagonist (droperidol and metoclopramide), muscarinic cholinergic Type 1 receptor antagonist (scopolamine), and histamine Type 1 receptor antagonist (promethazine and prochlorperazine)
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dexamethasone can effectively prevent PONV7, 8, 9 induced by epidural morphine used to reduce postoperative pain
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The use of low-dose naltrexone (LDN) as a novel anti-inflammatory treatment for chronic... - 0 views
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At the low dosage level, naltrexone exhibits paradoxical properties, including analgesia and anti-inflammatory actions
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In addition to the antagonist effect on mu-opioid and other opioid receptors, naltrexone simultaneously has an antagonist effect on non-opioid receptors (Toll-like receptor 4 or TLR4) that are found on macrophages such as microglia
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Once activated, microglia produce inflammatory and excitatory factors that can cause sickness behaviors such as pain sensitivity, fatigue, cognitive disruption, sleep disorders, mood disorders, and general malaise
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The neuroprotective action appears to result when microglia activation in the brain and spinal cord is inhibited
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By suppressing microglia activation, naloxone reduces the production of reactive oxygen species and other potentially neuroexcitatory and neurotoxic chemicals
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LDN has been reported to reduce not only self-reported pain in that condition but also objective markers of inflammation and disease severity
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shared by Nathan Goodyear on 07 Jan 13
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The activity of bisphenol A depends on both the est... [Endocr J. 2002] - PubMed - NCBI - 0 views
www.ncbi.nlm.nih.gov/...12402979
bisphenol A ER estrogen receptor receptors hormone hormones agonist antagonist estrogen receptor BPA
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shared by Nathan Goodyear on 07 May 13
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Antiandrogenic effects of bisphenol A and nonylp... [Toxicol Sci. 2003] - PubMed - NCBI - 0 views
www.ncbi.nlm.nih.gov/...12805653
Bisphenol-A androgen receptor antagonist androgen receptor androgen receptor hormone hormones xenoestrogens xenoestrogen
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shared by Nathan Goodyear on 13 May 13
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Testosterone: a vascular hormone in health and disease - 0 views
joe.endocrinology-journals.org/...R47.full
testosterone hormone health disease hormones men male cardiovascular disease CVD
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Testosterone has beneficial effects on several cardiovascular risk factors, which include cholesterol, endothelial dysfunction and inflammation
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In clinical studies, acute and chronic testosterone administration increases coronary artery diameter and flow, improves cardiac ischaemia and symptoms in men with chronic stable angina and reduces peripheral vascular resistance in chronic heart failure.
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testosterone is an L-calcium channel blocker and induces potassium channel activation in vascular smooth muscle cells
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Animal studies have consistently demonstrated that testosterone is atheroprotective, whereas testosterone deficiency promotes the early stages of atherogenesis
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there is no compelling evidence that testosterone replacement to levels within the normal healthy range contributes adversely to the pathogenesis of CVD (Carson & Rosano 2011) or prostate cancer (Morgentaler & Schulman 2009)
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bidirectional effect between decreased testosterone concentrations and disease pathology exists as concomitant cardiovascular risk factors (including inflammation, obesity and insulin resistance) are known to reduce testosterone levels and that testosterone confers beneficial effects on these cardiovascular risk factors
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Achieving a normal physiological testosterone concentration through the administration of testosterone replacement therapy (TRT) has been shown to improve risk factors for atherosclerosis including reducing central adiposity and insulin resistance and improving lipid profiles (in particular, lowering cholesterol), clotting and inflammatory profiles and vascular function
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It is well known that impaired erectile function and CVD are closely related in that ED can be the first clinical manifestation of atherosclerosis often preceding a cardiovascular event by 3–5 years
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no decrease in the response (i.e. no tachyphylaxis) of testosterone and that patient benefit persists in the long term.
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free testosterone levels within the physiological range, has been shown to result in a marked increase in both flow- and nitroglycerin-mediated brachial artery vasodilation in men with CAD
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Clinical studies, however, have revealed either small reductions of 2–3 mm in diastolic pressure or no significant effects when testosterone is replaced within normal physiological limits in humans
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Endothelium-independent mechanisms of testosterone are considered to occur primarily via the inhibition of voltage-operated Ca2+ channels (VOCCs) and/or activation of K+ channels (KCs) on smooth muscle cells (SMCs)
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Testosterone increases the expression of endothelial nitric oxide synthase (eNOS) and enhances nitric oxide (NO) production
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In addition to direct effects on NOS expression, testosterone may also affect phosphodiesterase type 5 (PDE5 (PDE5A)) gene expression, an enzyme controlling the degradation of cGMP, which acts as a vasodilatory second messenger
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the significance of the action of testosterone on VSMC apoptosis and proliferation in atherosclerosis is difficult to delineate and may be dependent upon the stage of plaque development
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Several human studies have shown that carotid IMT (CIMT) and aortic calcification negatively correlate with serum testosterone
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acute responses appear to be AR independent, long-term AR-mediated effects on the vasculature have also been described, primarily in the context of vascular tone regulation via the modulation of gene transcription
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Several studies, however, have demonstrated that the vasodilatory actions of testosterone are not reduced by aromatase inhibition
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non-aromatisable DHT elicited similar vasodilation to testosterone treatment in arterial smooth muscle
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increased endothelial NOS (eNOS) expression and phosphorylation were observed in testosterone- and DHT-treated human umbilical vein endothelial cells
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Androgen deprivation leads to a reduction in neuronal NOS expression associated with a decrease of intracavernosal pressure in penile arteries during erection, an effect that is promptly reversed by androgen replacement therapy
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Observational evidence suggests that several pro-inflammatory cytokines (including interleukin 1β (IL1β), IL6, tumour necrosis factor α (TNFα), and highly sensitive CRP) and serum testosterone levels are inversely associated in patients with CAD, T2DM and/or hypogonadism
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TRT has been reported to significantly reduce TNFα and elevate the circulating anti-inflammatory IL10 in hypogonadal men with CVD
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testosterone treatment to normalise levels in hypogonadal men with the MetS resulted in a significant reduction in the circulating CRP, IL1β and TNFα, with a trend towards lower IL6 compared with placebo
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Research suggests that the expression of VCAM-1, as induced by pro-inflammatory cytokines such as TNFα or interferon γ (IFNγ (IFNG)) in endothelial cells, can be attenuated by treatment with testosterone
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Testosterone also inhibits the production of pro-inflammatory cytokines such as IL6, IL1β and TNFα in a range of cell types including human endothelial cells
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decreased inflammatory response to TNFα and lipopolysaccharide (LPS) in human endothelial cells when treated with DHT
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The key to unravelling the link between testosterone and its role in atherosclerosis may lay in the understanding of testosterone signalling and the cross-talk between receptors and intracellular events that result in pro- and/or anti-inflammatory actions in athero-sensitive cells.
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Both NFκB and AR act at the transcriptional level and have been experimentally found to be antagonistic to each other
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As the AR and NFκB are mutual antagonists, their interaction and influence on functions can be bidirectional, with inflammatory agents that activate NFκB interfering with normal androgen signalling as well as the AR interrupting NFκB inflammatory transcription
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prolonged exposure of vascular cells to the inflammatory activation of NFκB associated with atherosclerosis may reduce or alter any potentially protective effects of testosterone
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DHT and IFNγ also modulate each other's signalling through interaction at the transcriptional level, suggesting that androgens down-regulate IFN-induced genes
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(Simoncini et al. 2000a,b). Norata et al. (2010) suggest that part of the testosterone-mediated atheroprotective effects could depend on ER activation mediated by the testosterone/DHT 3β-derivative, 3β-Adiol
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TNFα-induced induction of ICAM-1, VCAM-1 and E-selectin as well as MCP1 and IL6 was significantly reduced by a pre-incubation with 3β-Adiol in HUVECs
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3β-Adiol also reduced LPS-induced gene expression of IL6, TNFα, cyclooxygenase 2 (COX2 (PTGS2)), CD40, CX3CR1, plasminogen activator inhibitor-1, MMP9, resistin, pentraxin-3 and MCP1 in the monocytic cell line U937 (Norata et al. 2010)
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This study suggests that testosterone metabolites, other than those generated through aromatisation, could exert anti-inflammatory effects that are mediated by ER activation.
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The authors suggest that DHT differentially effects COX2 levels under physiological and pathophysiological conditions in human coronary artery smooth muscle cells and via AR-dependent and -independent mechanisms influenced by the physiological state of the cell
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There are, however, a number of systematic meta-analyses of clinical trials of TRT that have not demonstrated an increased risk of adverse cardiovascular events or mortality
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The TOM trial, which was designed to investigate the effect of TRT on frailty in elderly men, was terminated prematurely as a result of an increased incidence of cardiovascular-related events after 6 months in the treatment arm
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trials of TRT in men with either chronic stable angina or chronic cardiac failure have also found no increase in either cardiovascular events or mortality in studies up to 12 months
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Evidence may therefore suggest that low testosterone levels and testosterone levels above the normal range have an adverse effect on CVD, whereas testosterone levels titrated to within the mid- to upper-normal range have at least a neutral effect or, taking into account the knowledge of the beneficial effects of testosterone on a series of cardiovascular risk factors, there may possibly be a cardioprotective action
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The effect of testosterone on human vascular function is a complex issue and may be dependent upon the underlying androgen and/or disease status.
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the majority of studies suggest that testosterone may display both acute and chronic vasodilatory effects upon various vascular beds at both physiological and supraphysiological concentrations and via endothelium-dependent and -independent mechanisms
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shared by Nathan Goodyear on 14 May 13
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Testosterone Induces Dilation of Canine Coronary Conductance and Resistance Arteries In... - 0 views
circ.ahajournals.org/...2614.abstract
testosterone vasodilation androgen receptor AR androgen receptor antagonist blockade antagonist male men
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shared by Nathan Goodyear on 01 Jun 16
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Depression, antidepressant medications, and risk of Clostridium difficileinfection | BM... - 0 views
bmcmedicine.biomedcentral.com/...1741-7015-11-121
depression anti-depressants C difficile clostridium difficile
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Exogenous androgens influence body c... [J Clin Endocrinol Metab. 1996] - PubMed - NCBI - 0 views
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Older study finds weak synthetic androgen improves weight loss in obese postmenopausal women. This study compared nandrolone decanoate to spironolactone--an androgen receptor antagonist. No change in glucose or insulin was seen. Hard to draw a strong conclusion from this study due to the comparison of a synthetic androgen versus an anti-androgen. This comparison could have exaggerated the benefit of androgen in these women.
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[Oxytocin and male sexual function]. [Zhonghua Nan Ke Xue. 2011] - PubMed - NCBI - 0 views
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Bisphenol A Exposure during Adulthood Alters Expression of Aromatase and 5α-R... - 0 views
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The Androgen 5α-Dihydrotestosterone and Its Metabolite 5α-Androstan-3β, 17β-D... - 0 views
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Sex steroid hormones are primarily responsible for sex difference in adult HPA function; androgens inhibit whereas estrogens enhance HPA axis activation after a stressor
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the PVN contains relatively high levels of AR (Bingaman et al., 1994; Zhou et al., 1994) and ERβ (Alves et al., 1998; Hrabovszky et al., 1998; Somponpun and Sladek, 2003) but is essentially devoid of ERα
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the nonaromatizable androgen DHT and the nonselective ER ligand E2 influence HPA reactivity by acting on neurons within or surrounding the PVN
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inhibitory action of DHT is detectable at both the level of hormone secretion as well as PVN c-fos mRNA expression
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the inhibition can be mimicked by the DHT metabolite 3β-diol and by the subtype selective ERβ agonist DPN
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the ability of the ER antagonist tamoxifen, but not the AR antagonist flutamide, to block the inhibitory actions of DHT, speaks to the intracellular mechanism by which this inhibitory signal might be transduced.
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the DHT metabolite 3β-diol and the ERβ-subtype-selective agonist DPN suppressed ACTH, corticosterone, and c-fos mRNA responses to restraint stress in a manner similar to DHT
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metabolism of DHT to 3β-diol and subsequent binding to ERβ can be inhibitory to HPA reactivity, and this is one possible mechanism for the action of DHT.
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Our data also suggest that E2 enhances the reactivity of the HPA axis to stress by acting on or near neurons of the PVN
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these studies suggest that ERβ, within the male hypothalamus, acts to inhibit the HPA axis and that the inhibitory effects of DHT may be, at least in part, via its intracellular conversion to 3β-diol and subsequent binding to ERβ
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Neurobiological effects of the green tea constituent theanine and its potential role in... - 0 views
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shared by Nathan Goodyear on 04 Nov 13
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Acta Pharmacologica Sinica - Progress in studies of huperzine A, a natural cholinestera... - 0 views
www.nature.com/...aps20061a.html
Huperzine-A Huperzine Alzheimer's disease brain NMDA organophosphate organophosphates
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This study found that Huperzine A improved memory deficits in elderly and those with Alzheimer's disease. Huperzine A is an acetylcholinisterase inhibitor, thereby increasing the neurotransmitter acetylcholine. Huperzine A has also been shown to be neuroprotective through its antagonistic action with the NMDA receptors. Huperzine A has been shown to be protective from organophosphate toxicity.
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shared by Nathan Goodyear on 24 Oct 11
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Effect of amlodipine, a calcium channel antagonist, on gonadal steroid - 0 views
www.dovepress.com/id-o-peer-reviewed-article-JEP
calcium channel blocker anti-hypertension anti-hypertensive medication low T testosterone
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Complete reversal of adult-onset isolated hypo... [Fertil Steril. 2006] - PubMed - NCBI - 0 views
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study finds restoration of HPA in men with low T. This was performed via clomid therapy at 25 to 50 mg daily for 4 months. Increase in pulsatile LH, increase in serum Testosterone levels, and increase in sexual function was found. Clomid restores HPA function that is suppressed from estrogen inhibition. In this case, clomid is function as an estrogen antagonist.