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Nathan Goodyear

Bisphenol A Promotes Human Prostate Stem-Progenitor Cell Self-Renewal and Increases In ... - 0 views

www.ncbi.nlm.nih.gov/...PMC3929731

BPA bisphenol A cancer prostate cancer prostate xenoestrogens

shared by Nathan Goodyear on 20 Apr 16 - No Cached
  • these findings show that estrogen stimulates human prostate epithelial stem cell self-renewal and progenitor cell amplification (prostasphere size), with the greatest effects observed at lower E2 doses.
  • Similar to E2, BPA increased prostasphere number and size with significant and maximal effects observed at 10 nM BPA
  • Taken together, these results provide strong evidence that, similar to E2, BPA increases stem cell self-renewal and progenitor amplification in normal human prostate epithelial cells
  • ...13 more annotations...
  • these findings provide further support that E2 and BPA maintain the stem-like state within the normal prostate epithelial cell population
  • Our previous findings demonstrated that normal prostate stem-progenitor cells within the prostaspheres expressed ERα and ERβ, implicating them as direct targets for E2 and BPA action
  • p-Akt and p-Erk, well established downstream targets of membrane-associated ERs
  • BPA and E2 had equimolar capacity for activation of these rapid signaling pathways in human prostaspheres, thus identifying a dynamic and robust signaling pathway initiated by low-dose BPA exposure in prostate stem-progenitor cells.
  • these findings indicate that both rapid membrane-initiated estrogen action and genomic ER signaling pathways are operative in human prostate progenitor cells.
  • these results document the fact that levels of bioactive BPA in the present study are similar to levels found in human umbilical cord blood and newborns in the general population
  • the present findings identify for the first time that in vivo exposure of the human prostate epithelium to low doses of BPA significantly increases the susceptibility of the human prostate epithelium to hormonal carcinogenesis.
  • The current study provides clear evidence that, similar to E2, normal human prostate stem and progenitor cells are direct targets for BPA action
  • Both hormones increased stem-like cell numbers in primary prostate epithelial cultures in a dose-dependent manner and augmented the number and size of 3-D cultured prostaspheres, markers of stem cell self-renewal and progenitor cell proliferation, respectively
  • signaling pathways engaged by estrogens through these separate receptors are multiple and complex, including both membrane-initiated signaling and genomic activation via ER transcriptional activity
  • Estrogen action is mediated by ERα and ERβ
  • the current results indicate that developmental exposure to BPA, at doses routinely found in humans, significantly increases the cancer risk in human prostate epithelium in response to elevated estrogen levels in an androgen-supported milieu. Because relative estrogen levels rise in aging men, we suggest that humans may be susceptible to BPA-driven prostate disease in a manner similar to that in the rodent models.
  • We propose that early-life perturbations in estrogen signaling including inappropriate exposure to BPA have the potential to amplify and modify the stem-progenitor cell populations within the human prostate gland and, in so doing, alter the normal homeostatic mechanisms that maintain a growth neutral state throughout life
  • Nathan Goodyear on 20 Apr 16
     
    Bisphenol A exposure in utero found to increase prostate cancer risk later in life.  This exposure occurred at typical life exposure levels as found in umbilical cord blood sampling,  This occurred through stem cell self-renewal and progenitor amplification
Nathan Goodyear

Exposure to Bisphenol A Prenatally or in Adulthood Promotes TH2 Cytokine Production Ass... - 0 views

www.ncbi.nlm.nih.gov/...PMC2290985

BPA plastics endocrine disruptor immune T reg cells

shared by Nathan Goodyear on 01 Jul 11 - No Cached
  • BPA promotes the development of TH2 cells in adulthood and both TH1 and TH2 cells in prenatal stages by reducing the number of regulatory T cells.
  • Bisphenol A (BPA), an estrogenic endocrine-disrupting chemical (EDC
  • BPA is one of the most widespread EDCs.
  • ...12 more annotations...
  • BPA antagonizes the actions of thyroid hormone
  • Prenatal exposure to BPA has been shown to alter a variety of reproductive endocrine parameters, such as testosterone and luteinizing hormone levels
  • arly onset of sexual maturation of female mice
  • imbalanced T-helper (TH)1/TH2 immune responses have been demonstrated on exposure to BPA
  • indicating that BPA exerted its effects by reducing the number of Treg cells.
  • Exposure to BPA by subcutaneous injection in adulthood significantly promoted antigen-stimulated production of IL-4, IL-10, and IL-13 in TH2-skewed
  • BPA can leak from the placenta and accumulate in the fetus
  • We showed that prenatal exposure to BPA increased the production of a TH1 cytokine, IFN-γ, and a TH2 cytokine, IL-4, after the offspring developed, suggesting that prenatal exposure to BPA can induce persistent immunologic effects lasting into adulthood.
  • These results are consistent with a previous report that fetal exposure to BPA augmented TH1 and TH2 immune responses
  • our results clearly demonstrate that the production of TH2 cytokines is promoted by BPA in adult mice and in offspring during developmental exposure.
  • The decrease of Treg cells would predispose to immune dysfunction in aged individuals, explaining their higher risk of immune-mediated diseases, cancer, and infections.
  • BPA might cause these diseases. Thus, avoiding exposure to or promoting the excretion of BPA and other EDCs would help in preventing diseases and adverse health effects.
  • Nathan Goodyear on 01 Jul 11
     
    BPA as endocrine disruptor and as immune disruptor
Nathan Goodyear

The long-term consequences of exposure to lead. [Isr Med Assoc J. 2009] - PubMed - NCBI - 0 views

www.ncbi.nlm.nih.gov/...20108558

heavy metals lead chelation exposure

shared by Nathan Goodyear on 18 Mar 14 - No Cached
  • Nathan Goodyear on 18 Mar 14
     
    Study discusses the long term consequences of chronic lead exposure.  Acute lead toxicity is not the only mechanism of lead toxicity.  Lead can be toxic in chronic exposure.  This study also touches on the aspect that serum levels on reveal recent exposure as challenge and chelation are the only way to draw out and eliminate the stored metals.  When individuals lack detoxification enzymes i.e. glutathione these metals promote more symptoms and/or disease.
Nathan Goodyear

Altering the Intestinal Microbiota during a Critical Developmental Window Has Lasting M... - 0 views

www.cell.com/...S0092-8674(14)00821-6

antibiotics obesity gut flora microbiome bacteria metabolism

shared by Nathan Goodyear on 20 Aug 14 - No Cached
  • Nathan Goodyear on 20 Aug 14
     
    Study finds antibiotics given in late-pregnancy and during first months of life led to obesity in mice via altered gut flora.  This timed exposure was equal to life-time exposure.  This study points to the timing of antibiotic exposure as the key.
Nathan Goodyear

MedLink - 0 views

www.medlink.com/medlinkcontent.asp

mercury Hg polyneuropathy CNS neuropathy

shared by Nathan Goodyear on 16 Mar 15 - Cached
  • Nathan Goodyear on 16 Mar 15
     
    Mercury exposure associated with polyneuropathy. Sensory is more recent exposure with long term exposure associated with motor.
Nathan Goodyear

Duration of gluten exposure in adult coeliac disease does not correlate with the risk f... - 0 views

www.ncbi.nlm.nih.gov/...PMC1728461

gluten exposure autoimmune disease Celiac celiac disease

shared by Nathan Goodyear on 09 Jul 14 - No Cached
  • Nathan Goodyear on 09 Jul 14
     
    Studies have shown increased risk of autoimmune disease with gluten exposure early in life in those with Celiac disease.  This study found no increase risk with gluten exposure later in life.
Nathan Goodyear

Ibuprofen alters human testicular physiology to produce a state of compensated hypogona... - 0 views

www.pnas.org/...1715035115.full

ibuprofen Testosterone epigenetics hormones low Testosterone low T

shared by Nathan Goodyear on 09 Jan 18 - No Cached
  • The levels of LH in the ibuprofen group had increased by 23% after 14 d of administration
  • This increase was even more pronounced at 44 d, at 33%
  • We found an 18% decrease (P = 0.056) in the ibuprofen group compared with the placebo group after 14 d (Fig. 1A) and a 23% decrease (P = 0.02) after 44 d (Fig. 1C). Taken together, these in vivo data suggest that ibuprofen induced a state of compensated hypogonadism during the trial, which occurred as early as 14 d and was maintained until the end of the trial at 44 d
  • ...27 more annotations...
  • We first investigated testosterone production after 24 and 48 h of ibuprofen exposure to assess its effects on Leydig cell steroidogenesis. Inhibition of testosterone levels was significant and dose-dependent (β = −0.405, P = 0.01 at 24 h and β = −0.664, P < 0.0001 at 48 h) (Fig. 2A) and was augmented over time
  • The AMH data show that the hypogonadism affected not only Leydig cells but also Sertoli cells and also occurred as early as 14 d of administration
  • Sertoli cell activity showed that AMH levels decreased significantly with ibuprofen administration, by 9% (P = 0.02) after 14 d (Fig. 1B) and by 7% (P = 0.05) after 44 d compared with the placebo group
  • Examination of the effect of ibuprofen exposure on both the ∆4 and ∆5 steroid pathways (Fig. 2B) showed that it generally inhibited all steroids from pregnenolone down to testosterone and 17β-estradiol; the production of each steroid measured decreased at doses of 10−5–10−4 M. Under control conditions, production of androstenediol and dehydroepiandrosterone (DHEA) was below the limit of detection except in one experiment with DHEA
  • Measuring the mRNA expression of genes involved in steroidogenesis in vitro showed that ibuprofen had a profound inhibitory effect on the expression of these genes (Fig. 3 B–D), consistent with that seen above in our ex vivo organ model. Taken together, these data examining effects on the endocrine cells confirm that ibuprofen-induced changes in the transcriptional machinery were the likely reason for the inhibition of steroidogenesis.
  • Suppression of gene expression concerned the initial conversion of cholesterol to the final testosterone synthesis. Hence, expression of genes involved in cholesterol transport to the Leydig cell mitochondria was impaired
  • A previous study reported androsterone levels decreased by 63% among men receiving 400 mg of ibuprofen every 6 h for 4 wk
  • We next examined the gene expression involved in testicular steroidogenesis ex vivo and found that levels of expression of every gene that we studied except CYP19A1 decreased after exposure for 48 h compared with controls
  • the changes in gene expression indicate that the transcriptional machinery behind the endocrine action of Leydig cells was most likely impaired by ibuprofen exposure.
  • Together, these data show that ibuprofen also directly impairs Sertoli cell function ex vivo by inhibiting transcription
  • ibuprofen use in men led to (i) elevation of LH; (ii) a decreased testosterone/LH ratio and, to a lesser degree, a decreased inhibin B/FSH ratio; and (iii) a reduction in the levels of the Sertoli cell hormone AMH
  • The decrease in the free testosterone/LH ratio resulted primarily from the increased LH levels, revealing that testicular responsiveness to gonadotropins likely declined during the ibuprofen exposure. Our data from the ex vivo experiments support this notion, indicating that the observed elevation in LH resulted from ibuprofen’s direct antiandrogenic action
  • AMH levels were consistently suppressed by ibuprofen both in vivo and ex vivo, indicating that this hormone is uncoupled from gonadotropins in adult men. The ibuprofen suppression of AMH further demonstrated that the analgesic targeted not only the Leydig cells but also the Sertoli cells, a feature encountered not only in the human adult testis but also in the fetal testis
  • ibuprofen displayed broad transcription-repression abilities involving steroidogenesis, peptide hormones, and prostaglandin synthesis
  • a chemical compound, through its effects on the signaling compounds, can result in changes in the testis at gene level, resulting in perturbations at higher physiological levels in the adult human
  • The analgesics acetaminophen/paracetamol and ibuprofen have previously been shown to inhibit the postexercise response in muscles by repressing transcription
  • Previous ex vivo studies on adult testis have indeed pointed to an antiandrogenicity, only on Leydig cells, of phthalates (41), aspirin, indomethacin (42), and bisphenol A (BPA) and its analogs
  • ibuprofen’s effects were not restricted to Leydig and Sertoli cells, as data showed that the expression of genes in peritubular cells was also affected
  • short-term exposure
  • In the clinical setting, compromised Leydig cell function resulting in increased insensitivity to LH is defined as compensated hypogonadism (4), an entity associated with all-cause mortality
  • compensated hypogonadic men present with an increased likelihood of reproductive, cognitive, and physical symptoms
  • an inverse relationship was recently reported between endurance exercise training and male sexual libido
  • AMH concentrations are lower in seminal plasma from patients with azoospermia than from men with normal sperm levels
  • inhibin B is a key clinical marker of reproductive health (32). The function of AMH, also secreted by Sertoli cells, and its regulation through FSH remain unclear in men
  • the striking dual effect of ibuprofen observed here on both Leydig and Sertoli cells makes this NSAID the chemical compound, of all the chemical classes considered, with the broadest endocrine-disturbing properties identified so far in men.
  • after administration of 600 mg of ibuprofen to healthy volunteers
  • 14 d or at the last day of administration at 44 d
  • Nathan Goodyear on 09 Jan 18
     
    ibuprofen alters genetic expression that results in decreased Testosterone production.
Nathan Goodyear

Blood Lead Levels and Death from All Causes, Cardiovascular Disease, and Cancer: Result... - 0 views

www.ncbi.nlm.nih.gov/...PMC1626441

lead exposure Pb heavy metals mortality blood levels death cardiovascular disease cancer NHANES III

shared by Nathan Goodyear on 16 Apr 12 - No Cached
  • Nathan Goodyear on 16 Apr 12
     
    NHANES III reveals increased risk of death from all causes, but particularly CVD and cancer in very small exposures to lead.  No lead exposure is safe.
Nathan Goodyear

Prenatal exposure to endocrine-disrupting chemicals linked to breast cancer - 0 views

www.sciencedaily.com/...100521102633.htm

prenatal exposure endocrine disrupting chemicals BPA DES breast cancer

shared by Nathan Goodyear on 20 Feb 11 - Cached
  • Prenatal Exposure to Endocrine-Disrupting Chemicals Linked to Breast Cancer
  • Nathan Goodyear on 20 Feb 11
     
    prenatal exposure to chemicals linked to increase risk of breast cancer
Nathan Goodyear

PRECLINICAL STUDY: Changes in central dopaminergic systems and morphine reward by prena... - 0 views

onlinelibrary.wiley.com/...full

bisphenol-A bisphenol A BPA dopamine mesolimbic lactation organogenesis prenatal exposure

shared by Nathan Goodyear on 10 Oct 11 - No Cached
  • Nathan Goodyear on 10 Oct 11
     
    great study that shows how BPA exposure has its largest impact on the mesolimbic/dopamine system during organogenesis and lactation periods.
Nathan Goodyear

ScienceDirect - Environmental Research : The effect of long-term low-dose lead exposure... - 0 views

www.sciencedirect.com/...S0013935105001477

thyroid hypothyroid T4 lead exposure

shared by Nathan Goodyear on 05 Jul 11 - No Cached
  • his study revealed that long-term low-level lead exposure may lead to reduced FT4 level without significant changes in TSH and T3 levels in adolescents even at low Pb-B levels.
  • Nathan Goodyear on 05 Jul 11
     
    low lead level exposure and thyroid dysfunction
Nathan Goodyear

Improvement in semen quality associated with decreasing occupational lead exposure - Vi... - 0 views

onlinelibrary.wiley.com/doi/10.1002/(SICI)1097-0274(199903)35:3<257::AID-AJIM5>3.0.CO;2-#/abstract

lead exposure

shared by Nathan Goodyear on 05 Jul 11 - No Cached
  • These results support the notion that occupational lead exposure at currently acceptable levels has a small adverse effect on sperm quality, especially sperm motility, and that this effect is at least partially reversible
  • Nathan Goodyear on 05 Jul 11
     
    Reducing lead exposure levels partially reverses male sperm quality
Nathan Goodyear

Chelation Therapy for Patients with Elevated Body Lead Burden and Progressive Renal Ins... - 0 views

www.annals.org/...7.short

lead burden toxicity chelation EDTA

shared by Nathan Goodyear on 05 Jul 11 - No Cached
  • helation therapy seems to slow the progression of renal insufficiency in patients with mildly elevated body lead burden.
  • implies that long-term exposure to low levels of environmental lead may be associated with impaired renal function in patients with chronic renal disease.
  • Nathan Goodyear on 05 Jul 11
     
    long-term lead exposure and body burden may be associated with renal dysfunction. Treatment of long-standing lead exposure with chelation benefits patients with renal dysfunction
Nathan Goodyear

Exposure to the Functional Bacterial Amyloid Protein Curli Enhances Alpha-Synuclein Agg... - 0 views

www.nature.com/srep34477

neurodegenerative disease amyloid alzheimer's disease Parkinson's disease gut gut flora gut microbiome gut microbiota gut-brain

shared by Nathan Goodyear on 06 Oct 16 - No Cached
  • Our work suggests that protein misfolding and immune activation in neurodegenerative disorders are triggered through cross-seeding by exposure to exogenous microbial amyloids in the nose, mouth and gut.
  • Streptococcus mutans, Staphlococcus aureus, Salmonella enterica, Mycobacterium tuberculosis and others
  • Gene homologs encoding curli were recently determined also in four phyla: Bacteroidetes, Proteobacteria, Firmicutes, and Thermodesulfobacteria
  • ...8 more annotations...
  • changes in the gut microbiota induced by antibiotics alter neuroinflammation and amyloid deposition in a mouse model of AD
  • Our data suggest that amyloid proteins in the microbiota are involved in the origination and maintenance of neurodegenerative disease.
  • exposure to bacteria producing a functional extracellular amyloid protein enhances aggregation of AS in brain neurons in aged rats and in muscle cells in nematodes
  • AS aggregates seed aggregation of tau
  • involvement of the vagus nerve in PD
  • microgliosis, astrogliosis and enhanced expression of IL-6, TLR2 and TNF in the brain following curli exposure suggest the occurrence of an enhanced local sterile inflammatory response to AS in the brain.
  • the immune system in both AD and PD have now been extensively established
  • TLR2 activation through exposure to bacterial amyloid is pathogenic
  • Nathan Goodyear on 06 Oct 16
     
    Gut bacteria may play crucial role in systemic inflammation that leads to Alzheimer's and Parkinson's disease.  These amyloid production bacteria trigger systemic inflammation that leads to microglia activation and amyloid in the brain.   More establishment of the gut-brain connection.  
Nathan Goodyear

The relationship between dioxins and... [Environ Health Prev Med. 2012] - PubMed - NCBI - 0 views

www.ncbi.nlm.nih.gov/...23114996

saliva salivary hormone hormones cortisol cortisone DHEA dioxin agent orange

shared by Nathan Goodyear on 14 Nov 12 - No Cached
  • Nathan Goodyear on 14 Nov 12
     
    Areas of high exposure of Dioxin in Vietnam found to have associated elevated salivary cortisol, cortisone, and DHEA.  Now, this can only be seen as an association, but they did find these elevations only in the "hot spots" and not in low exposure areas.
Nathan Goodyear

ScienceDirect.com - The Journal of Steroid Biochemistry and Molecular Biology - Estroge... - 0 views

www.sciencedirect.com/...S0960076011001518

xenoestrogen xenoestrogens prostate male hormone estrogen receptor estrogen receptor alpha ER alpha estrogen receptor receptors environmental chemicals drugs

shared by Nathan Goodyear on 07 Jan 13 - No Cached
  • Nathan Goodyear on 07 Jan 13
     
    low dose xenoestrogen exposure increases prostate growth and future disease through fetal exposure and increased ER alpha expression.
Nathan Goodyear

Organophosphate Pesticide Exposure and Attention in Young Mexican-American Children: Th... - 1 views

www.ncbi.nlm.nih.gov/...PMC3002198

pesticide exposure children ADHD organophosphate pediatrics

shared by Nathan Goodyear on 21 Feb 13 - No Cached
  • Nathan Goodyear on 21 Feb 13
     
    In utero organophosphate exposure linked to ADHD, especially in boys.
Nathan Goodyear

Glyphosate impairs male offspring reproductive ... [Arch Toxicol. 2012] - PubMed - NCBI - 0 views

www.ncbi.nlm.nih.gov/...22120950

glyphosate Roundup Testosterone xenoestrogen xenoestrogens endocrine disruptor Toxins

shared by Nathan Goodyear on 04 Jul 13 - No Cached
  • Nathan Goodyear on 04 Jul 13
     
    Probably one of the more disturbing aspects of glyphosate exposure. In utero exposure, lowers Testosterone levels and effects the masculinization process of the young boy.  Very disturbing.  Our boys are being altered before they are even born.
Nathan Goodyear

http://ehp.niehs.nih.gov/wp-content/uploads/advpub/2016/5/EHP205.acco.pdf - 0 views

ehp.niehs.nih.gov/...EHP205.acco.pdf

obesity bisphenol A BPA EDC toxins environmental toxins endocrine disrupting chemicals

shared by Nathan Goodyear on 08 Jun 16 - No Cached
  • Nathan Goodyear on 08 Jun 16
     
    mothers with BPA exposure and thus prenatal exposure, increases risk of obesity risk in child.
Nathan Goodyear

Arsenic Exposure and Prevalence of Type 2 Diabetes in US Adults, August 20, 2008, Navas... - 0 views

jama.ama-assn.org/...814.abstract

arsenic diabetes low-level exposure Type II 2

shared by Nathan Goodyear on 06 Dec 11 - No Cached
  • Nathan Goodyear on 06 Dec 11
     
    low levels of Arsenic exposure is associated with increase risk of diabetes
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