Reproductive Toxicology, Journal Year: 2010, Volume and Issue: 30(4), P. 532 - 539
Published: July 24, 2010
Language: Английский
Reproductive Toxicology, Journal Year: 2010, Volume and Issue: 30(4), P. 532 - 539
Published: July 24, 2010
Language: Английский
Nature Reviews Endocrinology, Journal Year: 2016, Volume and Issue: 13(3), P. 161 - 173
Published: Nov. 18, 2016
Language: Английский
Citations
774Philosophical Transactions of the Royal Society B Biological Sciences, Journal Year: 2009, Volume and Issue: 364(1526), P. 2097 - 2113
Published: June 15, 2009
Concern exists over whether additives in plastics to which most people are exposed, such as phthalates, bisphenol A or polybrominated diphenyl ethers, may cause harm human health by altering endocrine function through other biological mechanisms. Human data limited compared with the large body of experimental evidence documenting reproductive developmental toxicity relation these compounds. Here, we discuss current state evidence, well future research trends and needs. Because exposure assessment is often a major weakness epidemiological studies, utero exposures toxicants important, also provide original on maternal phthalates during after pregnancy ( n = 242). Phthalate metabolite concentrations urine showed weak correlations between pre- post-natal samples, though strength relationship increased when duration two samples decreased. levels tended be higher samples. In conclusion, there great need for more studies adverse effects associated plastic additives. Recent advances measurement biomarkers hold much promise improving data, but their utility must understood facilitate appropriate study design.
Language: Английский
Citations
758Reproductive Toxicology, Journal Year: 2007, Volume and Issue: 24(2), P. 131 - 138
Published: July 31, 2007
Language: Английский
Citations
707Philosophical Transactions of the Royal Society B Biological Sciences, Journal Year: 2009, Volume and Issue: 364(1526), P. 2079 - 2096
Published: June 15, 2009
Components used in plastics, such as phthalates, bisphenol A (BPA), polybrominated diphenyl ethers (PBDE) and tetrabromobisphenol (TBBPA), are detected humans. In addition to their utility an inadvertent characteristic of these chemicals is the ability alter endocrine system. Phthalates function anti-androgens while main action attributed BPA oestrogen-like activity. PBDE TBBPA have been shown disrupt thyroid hormone homeostasis PBDEs also exhibit anti-androgen action. Experimental investigations animals indicate a wide variety effects associated with exposure compounds, causing concern regarding potential risk human health. For example, spectrum following perinatal male rats phthalates has remarkable similarities testicular dysgenesis syndrome Concentrations foetal mouse within range unconjugated levels observed blood produced animal experiments. Finally, hormones essential for normal neurological development reproductive function. Human body burdens high prevalence, concentrations young children, group particularly sensitive exogenous insults, typically higher, indicating need decrease compounds.
Language: Английский
Citations
592Environmental Health Perspectives, Journal Year: 2012, Volume and Issue: 120(6), P. 779 - 789
Published: Feb. 1, 2012
There has been increasing interest in the concept that exposures to environmental chemicals may be contributing factors epidemics of diabetes and obesity. On 11-13 January 2011, National Institute Environmental Health Sciences (NIEHS) Division Toxicology Program (NTP) organized a workshop evaluate current state science on these topics public health concern.The main objective was develop recommendations for research agenda after completing critical analysis literature humans experimental animals exposed certain chemicals. The considered at were arsenic, persistent organic pollutants, maternal smoking/nicotine, organotins, phthalates, bisphenol A, pesticides. High-throughput screening data from 21st Century (Tox21) also as way potential cellular pathways generate -hypotheses testing which how might perturb biological processes related obesity.Overall, review existing identified linkages between several type 2 diabetes. support "developmental obesogen" hypothesis, suggests chemical increase risk obesity by altering differentiation adipocytes or development neural circuits regulate feeding behavior. effects most apparent when developmental exposure is combined with consumption high-calorie, high-carbohydrate, high-fat diet later life. Research 1 very limited. This lack gap. In this review, we outline major themes emerged discuss activities NIEHS/NTP undertaking address recommendations. serves an introduction upcoming series articles regarding specific outcomes more detail.
Language: Английский
Citations
585Reproductive Toxicology, Journal Year: 2011, Volume and Issue: 31(3), P. 363 - 373
Published: Jan. 24, 2011
Language: Английский
Citations
573Environmental Research, Journal Year: 2016, Volume and Issue: 151, P. 251 - 264
Published: Aug. 7, 2016
Language: Английский
Citations
527Toxicology Letters, Journal Year: 2007, Volume and Issue: 176(2), P. 149 - 156
Published: Nov. 20, 2007
Language: Английский
Citations
494Proceedings of the National Academy of Sciences, Journal Year: 2013, Volume and Issue: 110(24), P. 9956 - 9961
Published: May 28, 2013
Bisphenol A (BPA) is an estrogenic endocrine disruptor widely used in the production of plastics. Increasing evidence indicates that utero BPA exposure affects sexual differentiation and behavior; however, mechanisms underlying these effects are unknown. We hypothesized may disrupt epigenetic programming gene expression brain. Here, we provide maternal during pregnancy to environmentally relevant doses (2, 20, 200 µg/kg/d) mice induces sex-specific, dose-dependent (linear curvilinear), brain region-specific changes genes encoding estrogen receptors (ERs; ERα ERβ) estrogen-related receptor-γ juvenile offspring. Concomitantly, altered mRNA levels regulators DNA methyltransferase (DNMT) 1 DNMT3A cortex hypothalamus, paralleling receptors. Importantly, DNMT (males) hypothalamus (females) were associated with methylation gene. induced persistent, largely sex-specific on social anxiety-like behavior, leading disruption sexually dimorphic behaviors. Although postnatal care was mothers treated pregnancy, not found be mediated by care. However, our data suggest increased partially attenuate methylation. Overall, demonstrate low-dose prenatal lasting possibly underlie enduring function especially regarding phenotypes.
Language: Английский
Citations
466Environmental Health Perspectives, Journal Year: 2010, Volume and Issue: 118(9), P. 1243 - 1250
Published: May 18, 2010
Bisphenol A (BPA) is a widespread endocrine-disrupting chemical used as the base compound in manufacture of polycarbonate plastics. In humans, epidemiological evidence has associated BPA exposure adults with higher risk type 2 diabetes and heart disease.We examined action environmentally relevant doses on glucose metabolism mice during pregnancy impact these females later life. We also investigated consequences utero to metabolic parameters pancreatic function offspring.Pregnant were treated either vehicle or (10 100 microg/kg/day) days 9-16 gestation. Glucose experiments performed pregnant their offspring.BPA aggravated insulin resistance produced was decreased tolerance increased plasma insulin, triglyceride, leptin concentrations relative controls. Insulin-stimulated Akt phosphorylation reduced skeletal muscle liver BPA-treated gestation had long-term for mothers: 4 months post-partum, weighed more than untreated leptin, glycerol levels greater resistance. At 6 age, male offspring exposed tolerance, resistance, altered blood compared mothers. The islets Langerhans from presented Ca2+ signaling secretion. BrdU (bromodeoxyuridine) incorporation into insulin-producing cells progeny, yet beta-cell mass unchanged.Our findings suggest that may contribute disorders homeostasis be factor diabetes.
Language: Английский
Citations
453