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1

Dobrzyński, Maciej, Jan P. Madej, Anna Leśków, Małgorzata Tarnowska, Jacek Majda, Monika Szopa, Andrzej Gamian, and Piotr Kuropka. "The Improvement of the Adaptation Process of Tocopherol and Acetylsalicylic Acid in Offspring of Mothers Exposed to TCDD." Animals 11, no. 12 (December 1, 2021): 3430. http://dx.doi.org/10.3390/ani11123430.

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Dioxins are chemical compounds that may cause an inflammatory reaction. During dioxin-induced inflammation, generated reactive oxygen species lead to morphological changes in various tissues and in biochemical parameters. The aim of this study was to demonstrate the changes in the livers of rats whose mothers were exposed to dioxins and the protective role of α-tocopherol and acetylsalicylic acid in liver inflammation. The study material consisted of Buffalo rats who were the offspring of females treated with dioxin, dioxin + α-tocopherol, or dioxin + acetylsalicylic acid. Livers and blood sam
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2

Keke Hu, Nigel J. Bunce. "METABOLISM OF POLYCHLORINATED DIBENZO-p-DIOXINS AND RELATED DIOXIN-LIKE COMPOUNDS." Journal of Toxicology and Environmental Health, Part B 2, no. 2 (March 1999): 183–210. http://dx.doi.org/10.1080/109374099281214.

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3

Patrizi, Barbara, and Mario Siciliani de Cumis. "TCDD Toxicity Mediated by Epigenetic Mechanisms." International Journal of Molecular Sciences 19, no. 12 (December 18, 2018): 4101. http://dx.doi.org/10.3390/ijms19124101.

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Dioxins are highly toxic and persistent halogenated organic pollutants belonging to two families i.e., Polychlorinated Dibenzo-p-Dioxins (PCDDs) and Polychlorinated Dibenzo Furans (PCDFs). They can cause cancer, reproductive and developmental issues, damage to the immune system, and can deeply interfere with the endocrine system. Dioxins toxicity is mediated by the Aryl-hydrocarbon Receptor (AhR) which mediates the cellular metabolic adaptation to these planar aromatic xenobiotics through the classical transcriptional regulation pathway, including AhR binding of ligand in the cytosol, transloc
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4

Colquhoun, David R., Erica M. Hartmann, and Rolf U. Halden. "Proteomic Profiling of the Dioxin-Degrading BacteriumSphingomonas wittichiiRW1." Journal of Biomedicine and Biotechnology 2012 (2012): 1–9. http://dx.doi.org/10.1155/2012/408690.

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Sphingomonas wittichiiRW1 is a bacterium of interest due to its ability to degrade polychlorinated dioxins, which represent priority pollutants in the USA and worldwide. Although its genome has been fully sequenced, many questions exist regarding changes in protein expression ofS. wittichiiRW1 in response to dioxin metabolism. We used difference gel electrophoresis (DIGE) and matrix-assisted laser desorption/ionization mass spectrometry (MALDI-MS) to identify proteomic changes induced by growth on dibenzofuran, a surrogate for dioxin, as compared to acetate. Approximately 10% of the entire put
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5

Chernyak, Yury I., Alla P. Merinova, Andrey A. Shelepchikov, Sergey I. Kolesnikov, and Jean A. Grassman. "Impact of dioxins on antipyrine metabolism in firefighters." Toxicology Letters 250-251 (May 2016): 35–41. http://dx.doi.org/10.1016/j.toxlet.2016.04.006.

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6

Swigonska, Sylwia, Tomasz Molcan, Anna Nynca, and Renata E. Ciereszko. "The involvement of CYP1A2 in biodegradation of dioxins in pigs." PLOS ONE 17, no. 5 (May 26, 2022): e0267162. http://dx.doi.org/10.1371/journal.pone.0267162.

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2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) is one of the most harmful chemicals showing resistance to biodegradation. The majority of TCDD effects is mediated by the aryl hydrocarbon receptor (AhR) pathway. TCDD binding to AhR results in the activation of cytochrome P450 enzymes (CYP1A1, CYP1A2, CYP1B1) involved in dioxin biodegradation. The goal of the study was to explore the potential role of CYP1A2 in the metabolism of TCDD. We investigated a molecular structure of CYP1A2 and the binding selectivity and affinity between the pig CYP1A2 and: 1/ DiCDD or TCDD (dioxins differing in toxicity an
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7

Galimov, Sh N., A. Z. Abdullina, R. S. Kidrasova, and E. F. Galimova. "Level of dioxins and glutathione system status in semen of male patients with infertility." Kazan medical journal 94, no. 5 (October 15, 2013): 658–61. http://dx.doi.org/10.17816/kmj1913.

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Aim. To evaluate of contamination of ejaculate by polychlorinated Dibenzo-p-dioxins/furans and to analyze the glutathione system status in males with infertility. Methods. 168 infertile and 49 fertile men were examined. Semen analysis was made in accordance with the World Health Organization protocol. The semen levels of persistent organic pollutants (dioxins and furans) was determined by a combination of high-performance capillary gas chromatography and high-resolution mass spectrometry, glutathione-depended enzymes activity - by enzyme-linked immunosorbent assay. Results. It is found that th
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8

Hu, Keke, and Nigel J. Bunce. "Metabolism of polychlorinated dibenzo-p-dioxins by rat liver microsomes." Journal of Biochemical and Molecular Toxicology 13, no. 6 (1999): 307–15. http://dx.doi.org/10.1002/(sici)1099-0461(1999)13:6<307::aid-jbt4>3.0.co;2-p.

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9

Bock, Karl Walter. "Human and rodent aryl hydrocarbon receptor (AHR): from mediator of dioxin toxicity to physiologic AHR functions and therapeutic options." Biological Chemistry 398, no. 4 (April 1, 2017): 455–64. http://dx.doi.org/10.1515/hsz-2016-0303.

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Abstract Metabolism of aryl hydrocarbons and toxicity of dioxins led to the discovery of the aryl hydrocarbon receptor (AHR). Tremendous advances have been made on multiplicity of AHR signaling and identification of endogenous ligands including the tryptophan metabolites FICZ and kynurenine. However, human AHR functions are still poorly understood due to marked species differences as well as cell-type- and cell context-dependent AHR functions. Observations in dioxin-poisoned individuals may provide hints to physiologic AHR functions in humans. Based on these observations three human AHR functi
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10

Molcan, Tomasz, Sylwia Swigonska, Anna Nynca, Agnieszka Sadowska, Monika Ruszkowska, Karina Orlowska, and Renata E. Ciereszko. "Is CYP1B1 involved in the metabolism of dioxins in the pig?" Biochimica et Biophysica Acta (BBA) - General Subjects 1863, no. 2 (February 2019): 291–303. http://dx.doi.org/10.1016/j.bbagen.2018.09.024.

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11

Kasai, Noriyuki, Shin-ichi Ikushiro, Raku Shinkyo, Kaori Yasuda, Shinji Hirosue, Akira Arisawa, Hirofumi Ichinose, Hiroyuki Wariishi, and Toshiyuki Sakaki. "Metabolism of mono- and dichloro-dibenzo-p-dioxins by Phanerochaete chrysosporium cytochromes P450." Applied Microbiology and Biotechnology 86, no. 2 (January 19, 2010): 773–80. http://dx.doi.org/10.1007/s00253-009-2413-x.

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12

Shinkyo, Raku, Toshiyuki Sakaki, Miho Ohta, and Kuniyo Inouye. "Metabolic pathways of dioxin by CYP1A1: species difference between rat and human CYP1A subfamily in the metabolism of dioxins." Archives of Biochemistry and Biophysics 409, no. 1 (January 2003): 180–87. http://dx.doi.org/10.1016/s0003-9861(02)00366-1.

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13

Korkalainen, Merja, Elise Kallio, Anu Olkku, Katri Nelo, Joanna Ilvesaro, Juha Tuukkanen, Anitta Mahonen, and Matti Viluksela. "Dioxins interfere with differentiation of osteoblasts and osteoclasts." Bone 44, no. 6 (June 2009): 1134–42. http://dx.doi.org/10.1016/j.bone.2009.02.019.

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14

Rosińczuk, Joanna, Robert Dymarek, and Ireneusz Całkosiński. "Histopathological, Ultrastructural, and Immunohistochemical Assessment of Hippocampus Structures of Rats Exposed to TCDD and High Doses of Tocopherol and Acetylsalicylic Acid." BioMed Research International 2015 (2015): 1–13. http://dx.doi.org/10.1155/2015/645603.

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The effect of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) on central nervous system consists of changing expression of estrogen receptors, whereas the result of chronic inflammatory reaction caused by dioxin is occurrence of destructive changes in various organs connected with disturbed metabolism of connective tissue and damage of cells. The aim of the study was to determine the effect of dioxins on function, ultrastructure, and cytological and histological structure of hippocampus, particularly on expression of estrogen receptors in central nervous system as well as to define protective influ
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Inui, Hideyuki, Toshimasa Itoh, Keiko Yamamoto, Shin-Ichi Ikushiro, and Toshiyuki Sakaki. "Mammalian Cytochrome P450-Dependent Metabolism of Polychlorinated Dibenzo-p-dioxins and Coplanar Polychlorinated Biphenyls." International Journal of Molecular Sciences 15, no. 8 (August 13, 2014): 14044–57. http://dx.doi.org/10.3390/ijms150814044.

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16

Inouye, Kuniyo, Raku Shinkyo, Teisuke Takita, Miho Ohta, and Toshiyuki Sakaki. "Metabolism of Polychlorinated Dibenzo-p-dioxins (PCDDs) by Human Cytochrome P450-Dependent Monooxygenase Systems." Journal of Agricultural and Food Chemistry 50, no. 19 (September 2002): 5496–502. http://dx.doi.org/10.1021/jf020415z.

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17

Sulistyaningdyah, Woro Triarsi, Jun Ogawa, Qing-Shan Li, Raku Shinkyo, Toshiyuki Sakaki, Kuniyo Inouye, Rolf D. Schmid, and Sakayu Shimizu. "Metabolism of polychlorinated dibenzo-p-dioxins by cytochrome P450 BM-3 and its mutant." Biotechnology Letters 26, no. 24 (December 2004): 1857–60. http://dx.doi.org/10.1007/s10529-004-5317-y.

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18

Dietrich, Cornelia. "Antioxidant Functions of the Aryl Hydrocarbon Receptor." Stem Cells International 2016 (2016): 1–10. http://dx.doi.org/10.1155/2016/7943495.

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The aryl hydrocarbon receptor (AhR) is a transcription factor belonging to the basic helix-loop-helix/PER-ARNT-SIM family. It is activated by a variety of ligands, such as environmental contaminants like polycyclic aromatic hydrocarbons or dioxins, but also by naturally occurring compounds and endogenous ligands. Binding of the ligand leads to dimerization of the AhR with aryl hydrocarbon receptor nuclear translocator (ARNT) and transcriptional activation of several xenobiotic phase I and phase II metabolizing enzymes. It is generally accepted that the toxic responses of polycyclic aromatic hy
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19

Savvateeva, Daria, Jorge Numata, Robert Pieper, Helmut Schafft, Monika Lahrssen-Wiederholt, and Sascha Bulik. "Physiologically based toxicokinetic models and in silico predicted partition coefficients to estimate tetrachlorodibenzo-p-dioxin transfer from feed into growing pigs." Archives of Toxicology 94, no. 1 (November 14, 2019): 187–96. http://dx.doi.org/10.1007/s00204-019-02617-0.

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AbstractTetrachlorodibenzo-p-dioxin (TCDD) is a ubiquitous, toxic, persistent and bioaccumulative organic pollutant. TCDD can potentially enter the food chain through contaminated food of animal origin as a consequence of feed contamination. Prediction of the TCDD transfer from feed into animal products is thus important for human health risk assessment. Here, we develop several physiologically based toxicokinetic (PBTK) models of TCDD transfer from contaminated feed into growing pigs (Sus scrofa) exposed to doses ranging from 24.52 to 3269.25 ng of TCDD. We test the consequences of explicit d
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20

Dopkins, Nicholas, Wurood Hantoosh Neameh, Alina Hall, Yunjia Lai, Alex Rutkovsky, Alexa Orr Gandy, Kun Lu, Prakash S. Nagarkatti, and Mitzi Nagarkatti. "Effects of Acute 2,3,7,8-Tetrachlorodibenzo-p-Dioxin Exposure on the Circulating and Cecal Metabolome Profile." International Journal of Molecular Sciences 22, no. 21 (October 30, 2021): 11801. http://dx.doi.org/10.3390/ijms222111801.

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2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) is a polyhalogenated planar hydrocarbon belonging to a group of highly toxic and persistent environmental contaminants known as “dioxins”. TCDD is an animal teratogen and carcinogen that is well characterized for causing immunosuppression through activation of aryl hydrocarbon receptor (AHR). In this study, we investigated the effect of exposure of mice to an acute dose of TCDD on the metabolic profile within the serum and cecal contents to better define the effects of TCDD on host physiology. Our findings demonstrated that within the circulating meta
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21

Craig, Zelieann R., Wei Wang, and Jodi A. Flaws. "Endocrine-disrupting chemicals in ovarian function: effects on steroidogenesis, metabolism and nuclear receptor signaling." REPRODUCTION 142, no. 5 (November 2011): 633–46. http://dx.doi.org/10.1530/rep-11-0136.

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Endocrine-disrupting chemicals (EDCs) are exogenous agents with the ability to interfere with processes regulated by endogenous hormones. One such process is female reproductive function. The major reproductive organ in the female is the ovary. Disruptions in ovarian processes by EDCs can lead to adverse outcomes such as anovulation, infertility, estrogen deficiency, and premature ovarian failure among others. This review summarizes the effects of EDCs on ovarian function by describing how they interfere with hormone signaling via two mechanisms: altering the availability of ovarian hormones,
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22

Takiguchi, Tomoya, Hoa Thi Vu, and Yoshikazu Nishino. "Effects of Polychlorinated Dibenzo-p-dioxins, Polychlorinated Dibenzofurans, and Dioxin-like PCBs on Teeth and Bones in Animals and Humans." Toxics 11, no. 1 (December 21, 2022): 7. http://dx.doi.org/10.3390/toxics11010007.

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Bone metabolism is regulated by endocrine systems, so people exposed to polychlorinated dibenzo-p-dioxins and dibenzofurans (PCDD/Fs) may suffer adverse effects on bones and teeth. We reviewed previous publications in which effects of PCDD/Fs and dioxin-like polychlorinated biphenyls on the teeth and bones of animals and humans were found. The aim was to identify future research directions, particularly for epidemiological studies of populations exposed to PCDD/Fs in the environment. Exposure of fetuses to PCDD/Fs may affect odontogenesis, particularly enamel formation, but the effects of PCDD
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23

Tonack, Sarah, Karen Kind, Jeremy G. Thompson, Anna M. Wobus, Bernd Fischer, and Anne Navarrete Santos. "Dioxin Affects Glucose Transport via the Arylhydrocarbon Receptor Signal Cascade in Pluripotent Embryonic Carcinoma Cells." Endocrinology 148, no. 12 (December 1, 2007): 5902–12. http://dx.doi.org/10.1210/en.2007-0254.

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Intoxication by dioxins such as 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) leads, among other damages, to early embryo loss, fetal malformations, and cardiovascular toxicity. Apart from binding to the arylhydrocarbon receptor (AhR), the mechanism of TCDD-mediated embryo toxicity is still unclear. We investigated possible modes of a TCDD-mediated toxicity, particularly in glucose metabolism, in pluripotent P19 mouse embryonic carcinoma cells. Undifferentiated P19 cells were exposed to 1–100 nm TCDD and characterized for AhR signaling. For studying cell differentiation, P19 cells were exposed to
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Diani-Moore, Silvia, Tiago Marques Pedro, and Arleen B. Rifkind. "Organ-specific effects on glycolysis by the dioxin-activated aryl hydrocarbon receptor." PLOS ONE 15, no. 12 (December 15, 2020): e0243842. http://dx.doi.org/10.1371/journal.pone.0243842.

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Activation of the aryl hydrocarbon receptor (AHR) by the environmental toxin dioxin (2,3,7,8-tetrachlorodibenzo-p-dioxin, TCDD) causes diverse toxicities, including thymus atrophy and hepatosteatosis. The mechanisms by which AHR activation by TCDD leads to these toxicities are not fully understood. Here we studied the effects of TCDD on a major energy pathway, glycolysis, using the chick embryo close to hatching, a well-established model for studying dioxin toxicity. We showed that 24 hr of TCDD treatment causes changes in glycolysis in both thymus and liver. In thymus glands, TCDD decreased m
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Lai, K. P., M. H. Wong, and C. K. C. Wong. "Inhibition of CYP450scc expression in dioxin-exposed rat Leydig cells." Journal of Endocrinology 185, no. 3 (June 2005): 519–27. http://dx.doi.org/10.1677/joe.1.06054.

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Polychlorinated dibenzo-p-dioxins, such as 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) have been recognized as highly potent developmental and reproductive toxins. We have previously demonstrated effects of TCDD in modulating the expression of rat Sertoli cell secretory products and markers for cell–cell interaction. In this study, we examined the direct biological effects of TCDD in rat Leydig cell primary cultures. Mature rat Leydig cells were purified by Percoll gradient centrifugation and the cell purity was determined by 3β-hydroxysteroid dehydrogenase (3β-HSD) staining and a testosterone
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26

Van den Berg, Martin, Joost De Jongh, Hermann Poiger, and James R. Olson. "The Toxicokinetics and Metabolism of Polychlorinated Dibenzo-p-Dioxins (PCDDs) and Dibenzofurans (PCDFs) and Their Relevance for Toxicity." Critical Reviews in Toxicology 24, no. 1 (January 1994): 1–74. http://dx.doi.org/10.3109/10408449409017919.

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27

Leijs, Marike M., Janna G. Koppe, Thomas Vulsma, Kees Olie, Wim M. C. van Aalderen, Pim de Voogt, Juliette Legler, and Gavin W. ten Tusscher. "Alterations in the programming of energy metabolism in adolescents with background exposure to dioxins, dl-PCBs and PBDEs." PLOS ONE 12, no. 9 (September 12, 2017): e0184006. http://dx.doi.org/10.1371/journal.pone.0184006.

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28

Zhang, Xing, Jodi A. Flaws, Michael J. Spinella, and Joseph Irudayaraj. "The Relationship between Typical Environmental Endocrine Disruptors and Kidney Disease." Toxics 11, no. 1 (December 29, 2022): 32. http://dx.doi.org/10.3390/toxics11010032.

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Endocrine disrupting chemicals (EDCs) are exogenous substances that alter the endocrine function of an organism, to result in adverse effects on growth and development, metabolism, and reproductive function. The kidney is one of the most important organs in the urinary system and an accumulation point. Studies have shown that EDCs can cause proteinuria, affect glomeruli and renal tubules, and even lead to diabetes and renal fibrosis in animal and human studies. In this review, we discuss renal accumulation of select EDCs such as dioxins, per- and polyfluoroalkyl substances (PFAS), bisphenol A
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Wang, Shu-Li, Yu-Chen Chang, How-Ran Chao, Chien-Ming Li, Lih-Ann Li, Long-Yau Lin, and Olaf Päpke. "Body Burdens of Polychlorinated Dibenzo- p -dioxins, Dibenzofurans, and Biphenyls and Their Relations to Estrogen Metabolism in Pregnant Women." Environmental Health Perspectives 114, no. 5 (May 2006): 740–45. http://dx.doi.org/10.1289/ehp.8809.

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30

Romanenko, T. "Elemental status of the adaptive state of reindeer calves in the ecological conditions of the Bolshezemelskaya tundra." Proceedings of the Komi Science Centre of the Ural Division of the Russian Academy of Sciences, no. 6 (December 28, 2022): 13–22. http://dx.doi.org/10.19110/1994-5655-2022-6-13-22.

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The chemical composition of essential elements in the longissimus back muscle and liver of 7-8-month-old reindeer calves has been evaluated. Differences in the content of Ca, a positive relationship with Mg and Fe have been noted. The identified features of metabolism in calves bred in different environments, the determining factor of which are soil types in the stable functioning of the soil–plant–animal system, provide advantages of the physiological state of the organism. By the studies of 2020 and 2021, calves of the current year of birth, comprising 83 % of slaughter, accumulate toxic sub
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Goncharov, N. P., G. V. Katsiya, A. N. Nizhnik, A. D. Dobracheva, T. N. Todua, A. A. Britvin, and N. I. Verbovaya. "Reproductive function in adolescents and men living in the dioxin-contaminated area of the Samara region." Problems of Endocrinology 50, no. 1 (February 15, 2004): 26–29. http://dx.doi.org/10.14341/probl11300.

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The study was undertaken to assess a potential risk of the elevated levels of dioxins in the town of Chapayevsk on reproductive function in adolescents during sexual maturation and in adults. It was ascertained that there was a regular trend for retarded sexual development by the Tanner stages in the adolescents living in the polluted areas as compared with control individuals of the same age. The incidence of cryptorchidism, varicocele, and inguinal hernias was 2-3 times higher in the boys from Chapayevsk than in those from Samara. However, the level of gonadotropic hormone was much higher in
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Močnik, Mirjam, and Nataša Marčun Varda. "Obesogens in Children—An Uncharted Territory." Metabolites 11, no. 12 (December 17, 2021): 882. http://dx.doi.org/10.3390/metabo11120882.

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Obesogens are exogenous chemicals belonging to the group of endocrine-disrupting chemicals and are believed to interfere in obesity development. In children, several chemicals are under investigation, most commonly bisphenol A, phthalates, perfluorinated alkyl substances, and persistent organic pollutants, including organochlorinated pesticides, tributyltin, polychlorinated biphenyls and dioxins. Several associations have been studied between chemical exposure in utero and postnatally. Current opinion among researchers indicates that the obesogen theory is very likely; however, limited publish
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Gregoraszczuk, Ewa L., and Anna Ptak. "Endocrine-Disrupting Chemicals: Some Actions of POPs on Female Reproduction." International Journal of Endocrinology 2013 (2013): 1–9. http://dx.doi.org/10.1155/2013/828532.

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Persistent organic pollutants (POPs), such as polychlorinated dibenzo-p-dioxins (PCDDs) and dibenzofurans (PCDFs), polychlorinated biphenyls (PCBs), and polybrominated ethers (PBDEs), chloronaftalens (PCNs), and bisphenol A (BPA), are stable, lipophilic pollutants that affect fertility and cause serious reproductive problems, including ovotoxic action, lack of ovulation, premature ovarian failure (POF), or polycystic ovarian syndrome (PCOS). Most of the representatives of POPs influence the activation of transcription factors, not only activation of aromatic hydrocarbon receptor (AhR), but als
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Arinç, Emel, Alaattin Sen, and Azra Bozcaarmutlu. "Cytochrome P4501A and associated mixed-function oxidase induction in fish as a biomarker for toxic carcinogenic pollutants in the aquatic environment." Pure and Applied Chemistry 72, no. 6 (January 1, 2000): 985–94. http://dx.doi.org/10.1351/pac200072060985.

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Polycyclic aromatic hydrocarbons (PAHs), dioxins, dibenzofurans, and polychlorinated biphenyls (PCBs) present in polluted environment induce cytochrome P4501A (CYP1A) isozyme in fish, which in turn results in a marked increased production of carcinogenic metabolites from PAHs. The induction of hepatic CYP1A in fish by certain classes of chemicals has been suggested as an early warning system, a "most sensitive biological response" for assessing environmental contamination conditions. This has implications for human fish consumption, as well as for the health status of aquatic organisms. Correl
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35

Spink, David C., Judith A. Johnson, Steven P. Connor, Kenneth M. Aldous та John F. Gierthy. "Stimulation of 17β‐estradiol metabolism in MCF‐7 cells by bromochloro‐ and chloromethyl‐substituted dibenzo‐p‐dioxins and dibenzofurans: Correlations with antiestrogenic activity". Journal of Toxicology and Environmental Health 41, № 4 (квітень 1994): 451–66. http://dx.doi.org/10.1080/15287399409531856.

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36

Dasenbrock, C., H. Bittmann, T. Wiesmüller, M. Oehmke, M. Kietzmann, E. Eigenbrodt, H. Hagenmaier, and B. Schlatterer. "Bioaccumulation of tetra-through octachlorinated dibenzo-p-dioxins in two different mixtures and their biochemical effects on enzymes of carbohydrate metabolism in mice." Chemosphere 25, no. 7-10 (October 1992): 1159–64. http://dx.doi.org/10.1016/0045-6535(92)90123-9.

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37

Gore, A. C., V. A. Chappell, S. E. Fenton, J. A. Flaws, A. Nadal, G. S. Prins, J. Toppari, and R. T. Zoeller. "Executive Summary to EDC-2: The Endocrine Society's Second Scientific Statement on Endocrine-Disrupting Chemicals." Endocrine Reviews 36, no. 6 (December 1, 2015): 593–602. http://dx.doi.org/10.1210/er.2015-1093.

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Abstract This Executive Summary to the Endocrine Society's second Scientific Statement on environmental endocrine-disrupting chemicals (EDCs) provides a synthesis of the key points of the complete statement. The full Scientific Statement represents a comprehensive review of the literature on seven topics for which there is strong mechanistic, experimental, animal, and epidemiological evidence for endocrine disruption, namely: obesity and diabetes, female reproduction, male reproduction, hormone-sensitive cancers in females, prostate cancer, thyroid, and neurodevelopment and neuroendocrine syst
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Sato, Shoko, Hitoshi Shirakawa, Shuhei Tomita, Yusuke Ohsaki, Keiichi Haketa, Osamu Tooi, Noriaki Santo, et al. "Low-dose dioxins alter gene expression related to cholesterol biosynthesis, lipogenesis, and glucose metabolism through the aryl hydrocarbon receptor-mediated pathway in mouse liver." Toxicology and Applied Pharmacology 229, no. 1 (May 2008): 10–19. http://dx.doi.org/10.1016/j.taap.2007.12.029.

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Boas, Malene, Ulla Feldt-Rasmussen, Niels E. Skakkebæk, and Katharina M. Main. "Environmental chemicals and thyroid function." European Journal of Endocrinology 154, no. 5 (May 2006): 599–611. http://dx.doi.org/10.1530/eje.1.02128.

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There is growing evidence that environmental chemicals can disrupt endocrine systems. Most evidence originates from studies on reproductive organs. However, there is also suspicion that thyroid homeostasis may be disrupted. Several groups of chemicals have potential for thyroid disruption. There is substantial evidence that polychlorinated biphenyls, dioxins and furans cause hypothyroidism in exposed animals and that environmentally occurring doses affect human thyroid homeostasis. Similarly, flame retardants reduce peripheral thyroid hormone (TH) levels in rodents, but human studies are scarc
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Costa, Elaine Maria Frade, Poli Mara Spritzer, Alexandre Hohl, and Tânia A. S. S. Bachega. "Effects of endocrine disruptors in the development of the female reproductive tract." Arquivos Brasileiros de Endocrinologia & Metabologia 58, no. 2 (March 2014): 153–61. http://dx.doi.org/10.1590/0004-2730000003031.

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Environmental agencies have identified a growing number of environmental contaminants that have endocrine disrupting activity, and these can become a major public health problem. It is suggested that endocrine disruptors could account for the higher-than-expected increase in the prevalence of some non-communicable diseases, such as obesity, diabetes, thyroid diseases, and some cancers. Several endocrine Disrupting Chemicals (EDCs), such as pesticides, bisphenol A, phthalates, dioxins, and phytoestrogens, can interact with the female reproductive system and lead to endocrine disruption. Initial
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Marinković, Natalija, Daria Pašalić, Goran Ferenčak, Branka Gršković, and Ana Rukavina. "Dioxins and Human Toxicity." Archives of Industrial Hygiene and Toxicology 61, no. 4 (December 1, 2010): 445–53. http://dx.doi.org/10.2478/10004-1254-61-2010-2024.

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Dioxins and Human ToxicityThe term dioxins usually refers to polychlorinated dibenzo-dioxins (PCDDs) and polychlorinated dibenzofurans (PCDFs). As 2,3,7,8-tetrachloro-dibenzo-p-dioxin (TCDD) has the highest toxic potential, the toxic potentials of other PCDDs and PCDFs are defined in comparison with it. Human exposure to dioxins can be environmental (background), occupational, or accidental pollution. In the human body, dioxins are in part metabolised and eliminated, and the rest is stored in body fat. People vary in their capacity to eliminate TCDD, but it is also dose-dependent; the eliminat
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Evteeva, A. A., M. S. Sheremeta, and E. A. Pigarova. "Endocrine disruptors in the pathogenesis of socially significant diseases such as diabetes mellitus, malignant neoplasms, cardiovascular diseases, pathology of the reproductive system." Obesity and metabolism 18, no. 3 (October 22, 2021): 327–35. http://dx.doi.org/10.14341/omet12757.

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Some environmental chemicals capable of interfering with the endocrine regulation of energy metabolism and the structure of adipose tissue in the function of the reproductive, immune, cardiovascular and other systems are called endocrine disruptors or disruptors. According to the WHO definition, the term «endocrine disruptors» means: «Exogenous substances or mixtures thereof that alter the function (s) of the endocrine system and, as a result, cause adverse effects in the intact organism or in its offspring, or (sub) population.» This includes compounds to which humanity is exposed in daily li
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Kawai, Shin'ichiro, M. Kobayashi, and Hideo Kaneko. "Effects of endocrine active substances in wildlife species: Genetic, biochemical, and physiological factors in variable susceptibility to endocrine disruptors." Pure and Applied Chemistry 75, no. 11-12 (January 1, 2003): 2335–41. http://dx.doi.org/10.1351/pac200375112335.

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Responses to endocrine active substances (EASs) in animals are various, and differences between the responses among individuals, populations and species are well known. These differences are observed not only in EASs but in most environmental chemicals including synthetic and naturally occurring ones. The basic differences in sensitivity to EASs are attributed to that of affinity or specificity of the receptors to EASs at the cellular level. Although the nucleotide sequences encoding for estrogen receptor proteins have been documented in several species and the functions of the receptors are t
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Cano, Raquel, José Pérez, Lissé Dávila, Ángel Ortega, Yosselin Gómez, Nereida Valero-Cedeño, Heliana Parra, et al. "Role of Endocrine-Disrupting Chemicals in the Pathogenesis of Non-Alcoholic Fatty Liver Disease: A Comprehensive Review." International Journal of Molecular Sciences 22, no. 9 (May 1, 2021): 4807. http://dx.doi.org/10.3390/ijms22094807.

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Non-alcoholic fatty liver disease (NAFLD) is considered the most common liver disorder, affecting around 25% of the population worldwide. It is a complex disease spectrum, closely linked with other conditions such as obesity, insulin resistance, type 2 diabetes mellitus, and metabolic syndrome, which may increase liver-related mortality. In light of this, numerous efforts have been carried out in recent years in order to clarify its pathogenesis and create new prevention strategies. Currently, the essential role of environmental pollutants in NAFLD development is recognized. Particularly, endo
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Ardag Akdogan, H., and A. Sen. "Characterization of drug metabolizing enzymes and assessment of aging in the gilthead seabream (Sparus aurata) liver." Veterinární Medicína 55, No. 9 (October 7, 2010): 463–71. http://dx.doi.org/10.17221/2982-vetmed.

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Organic anthropogenic compounds such as polycyclic aromatic hydrocarbons, polychlorinated biphenyls, nitroaromatics, dioxins, various pesticides and natural compounds can enter the aquatic environment. These lipophilic compounds are readily taken up into the tissues of aquatic organisms where biotransformation via Phase I and Phase II metabolism can in part, determine the fate and toxicity of the xenobiotics. In this study on gilthead seabream (Sparus aurata), liver microsomal ethoxyresorufin O-deethylase (EROD), methoxyresorufin O-demethylase (MROD), penthyloxyresorufin O-depenthylase (PROD),
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Vogeley, Christian, Charlotte Esser, Thomas Tüting, Jean Krutmann, and Thomas Haarmann-Stemmann. "Role of the Aryl Hydrocarbon Receptor in Environmentally Induced Skin Aging and Skin Carcinogenesis." International Journal of Molecular Sciences 20, no. 23 (November 28, 2019): 6005. http://dx.doi.org/10.3390/ijms20236005.

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The skin is constantly exposed to a variety of environmental threats, including solar electromagnetic radiation, microbes, airborne particulate matter, and chemicals. Acute exposure to these environmental factors results in the activation of different signaling pathways that orchestrate adaptive stress responses to maintain cell and tissue homeostasis. Chronic exposure of skin to these factors, however, may lead to the accumulation of damaged macromolecules and loss of cell and tissue integrity, which, over time, may facilitate aging processes and the development of aging-related malignancies.
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Brennan, Edwina, Thomas Keith Cunningham, Thozhukat Sathyapalan, and Stephen Lawrence Atkin. "The Association of the Polychlorinated Biphenyl Class of Endocrine Disruptors With Polycystic Ovary Syndrome and Thyroid Dysfunction." Journal of the Endocrine Society 5, Supplement_1 (May 1, 2021): A492. http://dx.doi.org/10.1210/jendso/bvab048.1006.

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Abstract Introduction:. Polychlorinated biphenyls (PCBs) are a class of endocrine disruptors with a long half-life in the body that are associated with irregular menses, growth and development delay, increased cancer risk, thyroid disorders and an increased risk of diabetes. Higher levels of PCBs have been related to polycystic ovary syndrome (PCOS). PCB toxicity depends on their structure, with coplanar PCBs being most toxic (akin to dioxins); therefore, PCB subtypes were determined to see if they differed in women with PCOS compared to normal controls. Methods:. PCB levels were compared in C
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Zawatski, William, and Mary M. Lee. "Male pubertal development: are endocrine-disrupting compounds shifting the norms?" Journal of Endocrinology 218, no. 2 (May 24, 2013): R1—R12. http://dx.doi.org/10.1530/joe-12-0449.

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Endocrine-disrupting compounds (EDCs) are synthetic or natural compounds that interfere with endogenous endocrine action. The frequent use of chemicals with endocrine active properties in household products and contamination of soil, water, and food sources by persistent chemical pollutants result in ubiquitous exposures. Wildlife observations and animal toxicological studies reveal adverse effects of EDCs on reproductive health. In humans, a growing number of epidemiological studies report an association with altered pubertal timing and progression. While these data are primarily reported in
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Bornstein, Stefan R., Karin Voit-Bak, Dieter Schmidt, Henning Morawietz, Alexander Benjamin Bornstein, Waldimir Balanzew, Ulrich Julius, et al. "Is There a Role for Environmental and Metabolic Factors Predisposing to Severe COVID-19?" Hormone and Metabolic Research 52, no. 07 (June 29, 2020): 540–46. http://dx.doi.org/10.1055/a-1182-2016.

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AbstractThe severe acute respiratory syndrome-coronavirus-2 (SARS-CoV-2) pandemic affects people around the world. However, there have been striking differences in the number of infected individuals and deaths in different countries. Particularly, within Central Europe in countries that are similar in ethnicity, age, and medical standards and have performed similar steps of containment, such differences in mortality rates remain inexplicable. We suggest to consider and explore environmental factors to explain these intriguing variations. Countries like Northern Italy, France, Spain, and UK hav
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Jorens, Philippe G., and Paul J. C. Schepens. "Human Pentachlorophenol Poisoning." Human & Experimental Toxicology 12, no. 6 (November 1993): 479–95. http://dx.doi.org/10.1177/096032719301200605.

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Pentachlorophenol (PCP) was, and still is, one of the most frequently used fungicides and pesticides, Its toxicity is due to interference with oxidative phosphorylation. Acute and chronic poisoning may occur by dermal absorption, inhalation or ingestion. Chronic poisoning occurs mainly in sawmill workers or people living in log homes treated with PCPcontaining wood protecting formulations. Quantitative determination of PCP in urine and serum is useful to detect occupational or subclinical exposure. The clinical features of acute and chronic PCP poisoning can be classified systematically into e
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