Browsing by Subject "hormones"
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Item ASSOCIATION BETWEEN PERFLUORONONANOIC ACID (PFNA) AND THYROID HORMONE LEVELS IN THE U.S. POPULATION: A CROSS-SECTIONAL STUDY OF NHANES DATA, 2007-2008(2014-03) Hall, Lauren R.; Cannell, Brad J.; Felini, MarthaPFNA is found in a wide array of consumer products, food, water, and air. Levels of PFNA in the environment continue to increase, and can accumulate over a lifetime. Thyroid hormones are responsible for regulating major processes of the human body. Decreasing levels of thyroid hormones could potentially interfere with essential metabolic processes. Results of this study help researchers better understand the levels of serum PFNA found in the U.S. general population, and adds to the growing body of knowledge of PFNA in relation to thyroid hormone levels. Purpose (a): Perfluorinated chemicals (PFCs) are widely used in many consumer products and have been linked with thyroid hormone disruption. Most studies have focused on perfluorooctonoic acid (PFOA) and perfluorooctane sulfonate (PFOS) exposures and thyroid hormone levels, but perfluoronananoic acid (PFNA) has shown to be associated with thyroid hormone levels in animal studies. More human studies are needed to assess PFNA in relation to thyroid hormone levels. We assessed the association between serum PFNA levels and serum thyroid hormone levels (T3, T4, and TSH) in the adult U.S general population. Methods (b): We analyzed data from the 2007-2008 National Health and Nutrition Examination Survey (NHANES) for participants 20 years of age and older. Sex-specific multivariable linear regression models were used to assess the association between perfluorononanoic acid (PFNA) and thyroid hormone measures of triiodothyronine (T3), thyroxine (T4), and thyroid stimulating hormone (TSH), separately, while adjusting for age, race, and BMI. Results (c): Higher concentrations of PFNA were found in males (males = 1.95 ng/mL and females = 1.60 ng/mL). There were statistically significant negative relationships with PFNA and T3 (p = 0.0013) and T4 (p = 0.0381) among males, after adjustment for age, race, and BMI, indicating that gender may be an effect modifier. Conclusions (d): PFNA is associated with decreasing T3 and T4 levels in males. However, there have been no consistent findings of an association between PFNA levels and thyroid hormone levels in previous studies. More evidence and research is needed to determine specific implications of PFNA exposure and thyroid function.Item Prospective Observational Study Evaluating Systemic Hormones and Corneal Crosslinking Effects in Keratoconus(Elsevier B.V., 2023-10-23) Van, Lyly; Bennett, Sashia; Nicholas, Sarah E.; Hjortdal, Jesper; McKay, Tina B.; Karamichos, DimitriosPURPOSE: To evaluate associations between hormone levels and corneal parameters in patients with keratoconus (KC), before and after photooxidative corneal collagen crosslinking (CXL). DESIGN: Prospective, observational cohort study. PARTICIPANTS: Twenty-eight patients with KC who were scheduled for CXL at Aarhus University Hospital in Denmark. METHODS: Androgen (dehydroepiandrosterone sulfate [DHEA-S]) and estrogen (estrone and estriol) plasma levels were measured and clinical assessments were performed before CXL and 2 to 3 months post-CXL, comparing the CXL eye with the control eye from the same participant. MAIN OUTCOME MEASURES: Associations between hormone levels and maximum corneal curvature (K(max)) and minimum central corneal thickness (CCt(min)) before and after CXL. RESULTS: Corneal collagen crosslinking was associated with a 2% reduction in K(max) values in the CXL eye, post-CXL, from baseline (median, 56.8 diopters [D]; 95% confidence interval [CI], 50.4-60.3) to the second visit (55.7 D; 95% CI, 50.4-58.8; P < 0.001). Systemic DHEA-S levels were 5 to 6 orders of magnitude higher than estriol or estrone concentrations in plasma. Importantly, estriol levels, rather than DHEA-S or estrone levels, were more closely correlated with K(max) before CXL (Spearman's r = 0.55, P = 0.01). Post-CXL K(max) and CCt(min) were not associated with DHEA-S, estrone, or estriol plasma levels at the same timepoint. CONCLUSIONS: This study provides supporting evidence based on a KC clinical population that systemic estrogen levels may influence corneal parameters (curvature and thickness) pre-CXL. Further studies evaluating the interplay between the therapeutic benefits of CXL and systemic hormone distributions are needed to determine if perturbation of the local corneal microenvironment influences endocrine function. FINANCIAL DISCLOSURES: The authors have no proprietary or commercial interest in any materials discussed in this article.Item Role of Serine/Threon protein Phosphateases in Estrogen Mediated Neuroprotection(2007-08-01) Yi, Kun DonThe Signaling pathways that mediate neurodegeneration are complex and involve a balance between phosphorylation and dephosphorylation of Signaling and Structural proteins. Estrogens have a variety of mode of action including transducing signaling events including the activation and/or supression of survival pathways. The purpose of this study was to delineate the role of protein phosphatases (PP) in estrogen neuroprotection. We assessed the role of PP in neuroprotection mediated by estrogen and its analogues. We also determined the role of estrogen receptors (ER) and MAPK signaling. Okadaic Acid (OA) and calyculin A (CA), non-specific serine/threonine PP inhibitors, were exposed to cells at various concentrations in the presence or absence of 17beta-estradiol, 17alpha-estradiol, the enantiomer of 17beta-estradiol (ENT E2), 2-(l-adamantyl)-3-hydroxyestra-1,3,5(10)-trien-17-one (ZYC3, non-ER binding estrogen analog) and/or glutamate. OA and CA caused a dose-dependent decrease in cell viability. None of the estrogen and its analogues showed protection against neurotoxic concentrations of either OA or CA, while all estrogens attenuated glutamate toxicity. However in the presence of these PP inhibitors, estrogen mediated protection against glutamate toxicity was lost. Glutamate treatment caused a 50% decrease in levels of PP1, PP2A and PP2B protein; while, co-administration of estrogen or its analogues with glutamate prevented the decrease in PP1, PP2A, and PP2B levels. In addition, PP2A and calcineurin activities were significantly suppressed with treatment of glutamate and/or OA; while the presence of these estrogens attenuated the decreases in PP activity. Moreover, an increase in reactive oxygen species, protein cabonylation, lipid peroxidation, caspase-3 activity, and mitochondrial dysfunction were evidence in both glutamate and OA mediated cell death. Estrogens attenuate these increases in glutamate-mediated cell death, but were ineffective in OA-induced neuronal death. Furthermore, gluatmate treatment caused a persistent increase in phosphorylation of ERK1/2 that corresponds with the decrease protein levels of PPs. Treatment of estrogens protect cells against glutamate-induced oxidative stress and excitotoxicity through an ER-independent mediated mechanism that serves to preserve phosphatase activity in the face of oxidative/excitotoxic insults resulting in attenuation of the persistent phosphorylation of ERK1/2 associated with neuronal death.