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Organic Chemicals
Published in William J. Rea, Kalpana D. Patel, Reversibility of Chronic Disease and Hypersensitivity, Volume 4, 2017
William J. Rea, Kalpana D. Patel
Other potential mechanisms of BPA toxicity may be relevant to the results presented here. Maxi-K channels and the β1 subunit in particular284 play key roles in regulating smooth muscle excitability and are estrogen sensitive. BPA in the micromolar range activates Maxi-K (kcal.1) ion channels in human coronary smooth muscle cells in culture to a degree sufficient to hyperpolarize the membrane potential.285 Laboratory exposure studies have shown that BPA can induce liver and oxidative cellular damage,286 disrupt pancreatic β-cell function,287 and have obesity-promoting effects,288 all of which could plausibly contribute toward CAD risk. Certain BPA derivatives, including bisphenol A diglycidyl ether (BADGE), are peroxisome proliferator-activated receptor-γ agonists, which may activate or inhibit ion channel activity in vessel walls directly,289 providing an alternative mechanism worthy of further investigation.
Reproductive and Developmental Toxicity Studies by Cutaneous Administration
Published in Rhoda G. M. Wang, James B. Knaak, Howard I. Maibach, Health Risk Assessment, 2017
Rochelle W. Tyl, Raymond G. York, James L. Schardein
A number of chemicals used in plastics manufacture have been investigated in animals during development by the cutaneous route. An epoxyresin, bisphenol A diglycidyl ether, induced only skin irritation in rabbits when applied at dosages of 30 to 300 mg/kg on gestational days 6 to 18.134
Endocrine Disrupting Chemicals, Obesogens, and the Obesity Epidemic
Published in Nathalie Bergeron, Patty W. Siri-Tarino, George A. Bray, Ronald M. Krauss, Nutrition and Cardiometabolic Health, 2017
Raquel Chamorro-Garcia, Bruce Blumberg, Nathalie Bergeron, Patty W. Siri-Tarino, George A. Bray, Ronald M. Krauss
The organotins tributyltin (TBT) and triphenyltin (TPT) were the first obesogens described and they both activate PPARγ (Grun et al. 2006, Janesick et al. 2016, Kanayama et al. 2005). More recently, the pesticides triflumizole, quinoxyfen, spirodiclofen, and zoxamide have been shown to activate PPARγ and to increase lipid accumulation using in vitro models such as the murine pre-adipocyte 3T3-L1 cell line and mouse and human mesenchymal stem cells (MSCs) (Janesick et al. 2016, Li et al. 2012). In the same study, we found that the fungicide fludioxonil is not a PPARγ activator, but it activates RXR and increases lipid accumulation in 3T3-L1 cells and MSCs (Janesick et al. 2016). MSCs are able to differentiate into a variety of cell types, including adipocytes, osteoblasts, chondrocytes, and myocytes, depending upon the stimuli they receive (Cristancho and Lazar 2011). By exposing 3T3-L1 cells or MSCs to obesogen candidates in the presence of an adipogenic cocktail, it is possible to assess the adipogenic capabilities of individual chemicals by analyzing lipid accumulation and mRNA expression levels of adipogenic marker genes such as those described earlier (Chamorro-Garcia et al. 2012, Grun et al. 2006, Janesick et al. 2016, Kirchner et al. 2010). There is a subset of candidate obesogens whose mechanisms of action remain unknown. One example is bisphenol-A diglycidyl ether (BADGE), which is used in the manufacture of epoxy resins, paints, and as a coating in food cans. BADGE induces lipid accumulation in 3T3-L1 pre-adipocytes and MSCs, but the inhibition of PPARγ with the specific antagonists T0070907 or GW9663 does not interfere with BADGE-induced accumulation of lipids (Chamorro-Garcia et al. 2012). Other potential obesogens whose mechanisms of action remain unknown are imazalil, tebupirimfos, florchlorfenuron, flusilazole, acetamiprid, and pymetrozine, which are not PPARγ or RXR activators but induce adipogenesis in 3T3-L1 cells (Janesick et al. 2016). These studies indicate that further analyses are needed to more fully understand the mechanisms through which obesogens act.
Substitution of bisphenol A: a review of the carcinogenicity, reproductive toxicity, and endocrine disruption potential of alternative substances
Published in Critical Reviews in Toxicology, 2020
Shalenie P. den Braver-Sewradj, Rob van Spronsen, Ellen V. S. Hessel
Bisphenol A (BPA, 2,2-bis(4-hydroxyphenyl)propane) is an industrial high production volume chemical that is widely used in the manufacture of polycarbonate, a rigid and transparent plastic. Polycarbonate is used as food contact material. BPA is also used to create bisphenol A diglycidyl ether (BADGE), the basic monomer unit in epoxy resins, which are used to protect canned food and beverages and as a surface-coating on drinking water storage tanks. Non-food-related applications of BPA include its use in toys, thermal paper and medical devices (Hormann et al. 2014; EFSA, CEF Panel 2015; SCENIHR 2015; Bakker et al. 2016). BPA is also found in cosmetics, probably due to migration from packages. Due to the broad application of BPA, exposure of the general population to BPA can occur via a range of products (EFSA, CEF Panel 2015; Boon et al. 2018).
Molecular interactions of bisphenols and analogs with glucocorticoid biosynthetic pathway enzymes: an in silico approach
Published in Toxicology Mechanisms and Methods, 2018
Garima Verma, Mohemmed Faraz Khan, Wasim Akhtar, Mohammad Mumtaz Alam, Mymoona Akhter, Mohammad Shaquiquzzaman
A set of 25 ligands (Table 2) was used for molecular docking studies including BPA, its analogs and known inhibitors of enzymes of GBP. Bisphenol ligands used in study were BPA, Bisphenol B (BP B), Bisphenol C (BP C), Bisphenol C2 (BP C2), Bisphenol E (BP E), BP F, Bisphenol G (BP G), BP M, BP P, BP S, Bisphenol Z (BP Z), Bisphenol AF (BP AF), Bisphenol AP (BP AP), Bisphenol BP (BP BP), Bisphenol A diglycidyl ether (BPA diglycidyl ether), Bisphenol PH (BP PH), Bisphenol TMC (BP TMC) and Tetrachloro bisphenol A (Tetrachloro BPA). Various known inhibitors of enzymes of GBP (listed in Table 1) were also included for docking studies to compare their binding affinities with those of BPA and its analogs. The three-dimensional coordinates of all the ligand structures were prepared using Maestro 10.5 GUI of Schrödinger 2016-1. All the ligands were prepared using LigPrep v3.1 module of Schrödinger. Epik v3.5 was used to expand protonation and tautomeric states at 7.0 ± 2.0 pH and energy was minimized using the OPLS_2005 force field.