Статті в журналах: "Dioxins Metabolism"

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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 samples were taken from the rats’ offspring, and then histopathological and biochemical analyses were performed. The histopathological analysis showed that the changes observed in the livers of neonates were the result of the dioxins derived from their mother. The biochemical analysis showed that the morphological changes in the liver affected its function, which manifested in a higher total protein concentration in the dioxin-treated group, and that the creatinine level in this group was significantly higher than that in the other groups. This effect was reduced by the protective role of α-tocopherol and acetylsalicylic acid. Based on these results, we came to the conclusion that dioxins significantly affect the structure of the liver, which negatively affects its function, mainly in the scope of the metabolism of plasma proteins and hepatic enzymes.

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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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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, translocation of the receptor to the nucleus, dimerization with the AhR nuclear translocator, and the binding of this heterodimeric transcription factor to dioxin-responsive elements which regulate the expression of genes involved in xenobiotic metabolism. 2,3,7,8-TCDD is the most toxic among dioxins showing the highest affinity toward the AhR receptor. Beside this classical and well-studied pathway, a number of papers are dealing with the role of epigenetic mechanisms in the response to environmental xenobiotics. In this review, we report on the potential role of epigenetic mechanisms in dioxins-induced cellular response by inspecting recent literature and focusing our attention on epigenetic mechanisms induced by the most toxic 2,3,7,8-TCDD.

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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 putative proteome of RW1 could be observed. Several components of the dioxin and dibenzofuran degradation pathway were shown to be upregulated, thereby highlighting the utility of using proteomic analyses for studying bioremediation agents. This is the first global protein analysis of a microorganism capable of utilizing the carbon backbone of both polychlorinated dioxins and dibenzofurans as the sole source for carbon and energy.

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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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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 and biodegradability) or 2/ their selected metabolites. pCYP1A2 demonstrated higher affinity towards DiCDD and TCDD than other pCYP1 enzymes. All dioxin-pCYP1A2 complexes were found to be stabilized by hydrophobic interactions. The calculated distances between the heme oxygen and the dioxin carbon nearest to the oxygen, reflecting the hydroxylating potential of CYP1A2, were higher than in other pCYP1 enzymes. The distances between the heme iron and the nearest dioxin carbon exceeded 5 Å, a distance sufficient to allow the metabolites to leave the active site. However, the molecular dynamics simulations revealed that two access channels of CYP1A2 were closed upon binding the majority of the examined dioxins. Moreover, the binding of dioxin metabolites did not promote opening of channel S–an exit for hydroxylated products. It appears that the undesired changes in the behavior of access channels prevail over the hydroxylating potential of CYP1A2 towards TCDD and the favorable distances, ultimately trapping the metabolites at the enzyme’s active site.

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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 the levels of priority environmental pollutants of dioxins and furans classes was 2,2-2,3 times higher in the semen of infertile men compared to fertile donors. The maximum level of the most toxic congener - 2,3,7,8-tetrachlorodibenzo-p-dioxin - was detected in patients pathospermia, which was found in most infertile patients. The glutathione redox system status in males with infertility was characterized by the decrease in the reduced tripeptide concentration, decreased activity of glutathione-depended xenobiotic detoxification enzymes (glutathione peroxidase and glutathione-S-transferase), multidirectional shifts of metabolism-mediating enzymes (inhibition of glutathione reductase associated with stimulation of g-glutamyltransferase). The molecular mechanisms of polychlorinated dioxins/furans toxicity for the male reproductive system are discussed, which may be mediated by redox state-sensitive signaling systems modulation. Conclusion. Contamination of semen in infertile men by environmental pollutants of polychlorinated dibenzo-p-dioxins and furans classes supports the hypothesis of the relationship of the reproductive pathology with environmental factors. The most important link in the pathogenesis of decreased fertility in men associated with anthropogenic pollution is the change of glutathione antioxidant/antitoxic system activity.

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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 functions are discussed: (1) Chemical defence and homeostasis of endobiotics. The AHR variant Val381 in modern humans leads to reduced AHR affinity to aryl hydrocarbons in comparison with Neanderthals and primates expressing the Ala381 variant while affinity to indoles remains unimpaired. (2) Homeostasis of stem/progenitor cells. Dioxins dysregulate homeostasis in sebocyte stem cells. (3) Modulation of immunity. In addition to microbial defence, AHR may be involved in a ‘disease tolerance defence pathway’. Further characterization of physiologic AHR functions may lead to therapeutic options.

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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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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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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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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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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 influence of tocopherol (TCP) and acetylsalicylic acid (ASA) on the decrease in activity of proinflammatory effects in central nervous system. It was shown that TCDD contributes to destructive and inflammatory changes along with demyelization of myelin sheaths and atrophy of estrogen receptors in hippocampus. Dioxin contributes to atrophy of estrogen receptors in hippocampus, in which also destructive and inflammatory changes were found along with demyelination of myelin sheaths. Histopathological and ultrastructural image of hippocampus areas in rats, in which both TCP and ASA were used, is characterized by poorly expressed degenerative changes and smaller inflammatory reactivity. Using both TCP and ASA has a protective effect on functions of central nervous system.

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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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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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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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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 hydrocarbons, dioxins, and structurally related compounds are mediated by activation of the AhR. A multitude of studies indicate that the AhR operates beyond xenobiotic metabolism and exerts pleiotropic functions. Increasing evidence points to a protective role of the AhR against carcinogenesis and oxidative stress. Herein, I will highlight data demonstrating a causal role of the AhR in the antioxidant response and present novel findings on potential AhR-mediated antioxidative mechanisms.

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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 dose-dependent absorption (DDA) versus the indirect effects of a self-induced liver metabolism (SIM). The DDA and SIM models showed similar fit to experimental data, although currently it is not possible to unequivocally make statement on a mechanistic preference. The performance of both toxicokinetic models was successfully evaluated using the 1999 Belgian case of contaminated fats for feeding. In combination with toxicokinetic models of other dioxin congeners, they can be used to formulate maximum allowance levels of dioxins in feedstuffs for pigs. Additionally, the implementation of in silico-predicted partition coefficients was explored as a useful alternative to predict TCDD tissue distribution in low-dose scenarios without recurring to animal experiments.

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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 metabolome following acute TCDD exposure, there was significant dysregulation in the metabolism of bioactive lipids, amino acids, and carbohydrates when compared with the vehicle (VEH)-treated mice. These widespread changes in metabolite abundance were identified to regulate host immunity via modulating nuclear factor-kappa B (NF-κB) and extracellular signal-regulated protein kinase (ERK1/2) activity and work as biomarkers for a variety of organ injuries and dysfunctions that follow TCDD exposure. Within the cecal content of mice exposed to TCDD, we were able to detect changes in inflammatory markers that regulate NF-κB, markers of injury-related inflammation, and changes in lysine degradation, nicotinamide metabolism, and butanoate metabolism, which collectively suggested an immediate suppression of broad-scale metabolic processes in the gastrointestinal tract. Collectively, these results demonstrate that acute TCDD exposure results in immediate irregularities in the circulating and intestinal metabolome, which likely contribute to TCDD toxicity and can be used as biomarkers for the early detection of individual exposure.

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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, and altering binding and activity of the hormone at the receptor level. Among the chemicals covered are pesticides (e.g. dichlorodiphenyltrichloroethane and methoxychlor), plasticizers (e.g. bisphenol A and phthalates), dioxins, polychlorinated biphenyls, and polycyclic aromatic hydrocarbons (e.g. benzo[a]pyrene).

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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/Fs on bone genesis are limited to palatine bone. Exposure to PCDD/Fs in milk may affect both teeth and bones, but the effects on bones may be reversible. Exposure to high PCDD/F concentrations even during adulthood may adversely affect teeth. Exposure to PCDD/Fs may induce osteogenesis and improve bone properties because the disrupting effects of PCDD/Fs cause bone remodeling and vitamin D activation. More studies involving humans are required to investigate previously found associations between the PCDD/F concentrations humans are exposed to and biological markers for teeth and bones, including metabolites of vitamin D.

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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 10 nm TCDD at stage of embryoid body formation, and analyzed on glucose metabolism and cardiac differentiation during the next 3 wk. TCDD treatment activated the AhR-signaling cascade within 1 h, confirmed by AhR translocation, induction of cytochrome P450 1A1 expression, and activation of the xenobiotic response element. Although cell viability and transcription of the cardiac marker protein α-myosin heavy chain were affected, TCDD did not inhibit the differentiation of P19 cells to pulsating cardiomyocytes. TCDD significantly down-regulated the expression levels of the glucose transporter (GLUT) isoforms 1 and 3. After 24-h TCDD treatment, GLUT1 was no longer localized in the plasma membrane of P19 cells. The impaired GLUT expression correlated with a lower glucose uptake in 5-d-old embryoid bodies. The TCDD effects were mediated by AhR, as shown by preculture with the AhR antagonist α-naphthoflavone. Our data demonstrate that an AhR-mediated disturbance in GLUT expression and insufficient glucose uptake may be major mechanisms in TCDD embryo toxicity.

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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 mRNAs for glycolytic genes and glucose transporters, glycolytic indices and levels of IL7 mRNA, phosphorylated AKT (pAKT) and HIF1A, stimulators of glycolysis and promoters of survival and proliferation of thymic lymphocytes. In contrast, in liver, TCDD increased mRNA levels for glycolytic genes and glucose transporters, glycolytic endpoints and pAKT levels. Similarly, increases by TCDD in mRNA levels for glycolytic genes and glucose transporters in human primary hepatocytes showed that effects in chick embryo liver pertain also to human cells. Treatment with the glycolytic inhibitor 2-deoxy-d-glucose exacerbated the effects on thymus atrophy by TCDD, supporting a role for decreased glycolysis in thymus atrophy by TCDD, but did not prevent hepatosteatosis. NAD+ precursors abolished TCDD effects on glycolytic endpoints in both thymus and liver. In summary, we report here that dioxin disrupts glycolysis mediated energy metabolism in both thymus and liver, and that it does so in opposite ways, decreasing it in the thymus and increasing it in the liver. Further, the findings support NAD+ boosting as a strategy against metabolic effects of environmental pollutants such as dioxins.

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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 induction assay. To examine TCDD-induced biological consequences, we measured the changes in the secretion of progesterone and testosterone, as well as transcript levels of some selected steroidogenic enzymes (i.e. StAR, P450scc, 3β-HSD and CYP17α), in TCDD/human chorionic gonadotropin (hCG) co-treated cells. Our results indicated that TCDD (0.2 or 2 ng/ml) treatment significantly suppressed hCG (5 or 10 ng/ml)-induced testosterone secretion. The suppressive effect aligned with a reduction of progesterone secretion (P<0.05), as well as a decrease of P450scc mRNA and protein expression (P<0.05). The mechanistic action of TCDD was found to be via the reduction of cellular cAMP levels in the hCG-treated cells. This observation was further confirmed, as the TCDD-mediated suppressive effect could be reversed by dibutyryl cAMP co-treatment. The data indicate that TCDD can modulate cAMP signaling in rat Leydig cells to affect the process of steroidogenesis.

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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 (BPA), and phthalates, and delineate how exposures to such EDCs cause renal lesions and diseases, including cancer. The regulation of typical EDCs with specific target genes and the activation of related pathways are summarized.

29

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 substances, radionuclides and dioxins in muscle tissue, liver and kidneys within the agreed health-based exposure limits as they grow and develop under technogenic load of the Bolshezemelskaya tundra. Among the heavy metals studied (Cd, Hg, Pb, As), Pb and As concentrations in calves have low values of maximum permissible concentrations.

31

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 the Chapayevsk adolescents than that in the control group. Polluted area-living males with normal levels of reproductive hormones showed a drastic deterioration in the quality of sperm, mainly the morphological index with a characteristic reduction of the acrosomal area of the head of spermatozoons. They also displayed a decrease in the levels of dehydroepiandrosterone (DHEA) sulfate and increases in the level of cortisol and in cortisol/ DHEA sulfate ratios. The above deviations in the balance of corticosteroids suggest impaired adaptive homeostasis, which is one of the mechanisms responsible for a potential human health risk of polychlorinated hydrocarbons.

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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 published studies show inconsistent support for the obesogenic effects of most substances in children and are limited by difficulty in providing the exact mechanisms of action, nor is their mutual effect in humans known, let alone in children. Existing data indicate that we have only scratched the surface and have much more to learn about obesogens. Hopefully, in the future, more information will provide an opportunity for policy makers to take action and protect public health.

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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 also the steroid hormone receptors. This minireview will focus on a variety of PAH activities in oocyte, ovary, placenta, and mammary gland. The complexity and diversity of factors belonging to POPs and disorders of the reproductive function of women indicate that the impact of environmental pollution as an important determinant factor in fertility should not be minimize.

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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. Correlation between elevated CYP1A and altered steroid metabolism and decreased reproductive success has been pointed out. The induction of CYP1A and associated enzyme activities has now been confirmed in a number of field studies. Cases where these biomarkers have been studied in field conditions will be presented. Special emphasis will be given to field studies in which the induction of CYP1A activity, 7-ethoxyresorufin O-deethylase (EROD) activities and immunochemical detection of CYP1A in leaping mullet and common sole are used as a biomarker for PAH- and/or PCB-type pollutants along the Izmir Bay on the Aegean Sea.

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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 systems. EDCs such as bisphenol A, phthalates, pesticides, persistent organic pollutants such as polychlorinated biphenyls, polybrominated diethyl ethers, and dioxins were emphasized because these chemicals had the greatest depth and breadth of available information. The Statement also included thorough coverage of studies of developmental exposures to EDCs, especially in the fetus and infant, because these are critical life stages during which perturbations of hormones can increase the probability of a disease or dysfunction later in life. A conclusion of the Statement is that publications over the past 5 years have led to a much fuller understanding of the endocrine principles by which EDCs act, including nonmonotonic dose-responses, low-dose effects, and developmental vulnerability. These findings will prove useful to researchers, physicians, and other healthcare providers in translating the science of endocrine disruption to improved public health.

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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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39

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 scarce. Studies also indicate thyroid-disruptive properties of phthalates, but the effect of certain phthalates seems to be stimulative on TH production, contrary to most other groups of chemicals. Thyroid disruption may be caused by a variety of mechanisms, as different chemicals interfere with the hypothalamic–pituitary–thyroid axis at different levels. Mechanisms of action may involve the sodium–iodide symporter, thyroid peroxidase enzyme, receptors for THs or TSH, transport proteins or cellular uptake mechanisms. The peripheral metabolism of the THs can be affected through effects on iodothyronine deiodinases or hepatic enzymes. Even small changes in thyroid homeostasis may adversely affect human health, and especially fetal neurological development may be vulnerable. It is therefore urgent to clarify whether the animal data showing effects of chemicals on thyroid function can be extended to humans.

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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. Initially, it was assumed that EDCs exert their effects by binding to hormone receptors and transcription factors, but it is currently known that they may also alter the expression of enzymes involved in the synthesis or catabolism of steroids. Biomonitoring studies have identified these compounds in adults, children, pregnant women, and fetuses. Among the diseases of the female reproductive tract associated with EDCs exposure are the following: precocious puberty, polycystic ovary syndrome, and premature ovarian failure. The different populations of the world are exposed to a great number of chemicals through different routes of infection; despite the various available studies, there is still much doubt regarding the additive effect of a mixture of EDCs with similar mechanisms of action.

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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 elimination rate is much faster at higher than lower levels. The liver microsomal P4501A1 enzyme oxygenates lipophilic chemicals such as dioxins. It is encoded by the CYP1A1 gene. Cytosolic aryl hydrocarbon receptor (AhR) mediates their carcinogenic action. It binds to dioxin, translocates to nucleus and together with hydrocarbon nuclear translocator (ARNT) and xenobiotic responsive element (XRE) increases the expression of CYP1A1.Dioxins are classified as known human carcinogens, but they also cause noncancerous effects like atherosclerosis, hypertension, and diabetes. Long-term exposures to dioxins cause disruption of the nervous, immune, reproductive, and endocrine system. Short-term exposure to high levels impairs the liver function and causes chloracne. The most sensitive population to dioxin exposure are the foetuses and infants.A large number of health effects have been documented in the scientific literature, and they all place dioxins among the most toxic chemicals known to man.

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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 life as a result of their use in pesticides, herbicides, industrial and household products, plastics, detergents, refractory impregnations and as ingredients in personal care products. This review will present the latest scientific data on various ERs, such as persistent organic pollutants (POPs): pesticides (mirex, chlordecane, endosulfan, hexachlorobenzene-HCB dichlorodiphenyltrichloroethane-DDT and its metabolites), industrial chemicals (bisphenol A, polybrominated ether -PBDE, polychlorinated biphenyls-PCB, nonylphenol, dioxins, perfluorooctanoic acid-PFOA, phthalates), pharmaceuticals (diethylstilbestrol-DES). ERs are regarded as compounds that cause obesity, since they have the ability to influence cellular processes associated with adipose tissue, initiating changes in lipid metabolism and adipogenesis. Analysis of scientific materials on this issue indicates that ERs are ubiquitous in the environment and have a detrimental effect on the health of animals and mankind. The scientific and practical interest in this article is based on the growing statistics of the development of such socially significant pathologies as obesity and related diseases, including diabetes mellitus, metabolic syndrome, cardiovascular diseases, menstrual irregularities, as well as cancer and infertility, for of which obesity is a risk factor.

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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 the same, the ability to bind the natural hormones and the estrogenic xenobiotics is not necessarily identical. The reproductive endocrine system is basically common among vertebrates, but chemical types of hormones, physiological roles of hormones and the basal blood levels of hormones differ among each species, especially in sex steroids. These differences cause various types of responses and sensitivity to EASs among animal species. Xenobiotic metabolism is important for the genetical, biochemical and physiological factors concerning the influence of EASs. Some EASs directly inhibit cytochrome P450 (CYP) activity as was reported in tributyltin that inhibits CYP19 (aromatase) activity causing imposex in neogastropods. Some organochlorines including dioxins stimulate aryl hydrocarbon (Ah) receptor-mediated xenobiotic metabolism, and result in the metabolic disruption of steroid hormones such as estrogen as were reported in eggshell thinning in birds of prey and uterus occlusion in seals. CYP activity greatly differs among wildlife species in both terrestrial and aquatic organisms, and these differences are significantly responsible for the multiple effects or toxicity of EASs. Sex and age differences also cause different responses to EASs and are largely due to the differences in xenobiotic metabolizing activities.

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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, endocrine-disrupting chemicals (EDCs) have a notable influence. EDCs can be classified as natural (phytoestrogens, genistein, and coumestrol) or synthetic, and the latter ones can be further subdivided into industrial (dioxins, polychlorinated biphenyls, and alkylphenols), agricultural (pesticides, insecticides, herbicides, and fungicides), residential (phthalates, polybrominated biphenyls, and bisphenol A), and pharmaceutical (parabens). Several experimental models have proposed a mechanism involving this group of substances with the disruption of hepatic metabolism, which promotes NAFLD. These include an imbalance between lipid influx/efflux in the liver, mitochondrial dysfunction, liver inflammation, and epigenetic reprogramming. It can be concluded that exposure to EDCs might play a crucial role in NAFLD initiation and evolution. However, further investigations supporting these effects in humans are required.

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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), benzyloxyresorufin O-debenzylase (BROD), aniline 4-hydroxylase (A4H), N-nitrosodimethylamine N-demethylase (NDMA-DE), aminopyrine N-demethylase (APND), caffeine N-demethylase (CN3D) and erythromycin N-demethylase (ERND) were determined. A4H, ERND, NDMA-ND, EROD and PROD activities increased in gilthead seabream (Sparus aurata) liver microsomes of different ages, while CN3D and APND activities decreased. MROD activities were barely detectable in mature fish whereas BROD activities were not detectable at all ages studied. Results were also recorded at the protein level by Western blotting using anti-CYP1A, CYP2E and CYP3A antibodies. In conclusion, elevated levels of gilthead seabream liver microsomal CYP450 enzyme activities might reveal possible exposure to various exogenous compounds, which might affect the desired responses to drugs, hormones and dietary supplements used during breeding.

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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. One transcription factor that is expressed in all cutaneous cells and activated by various environmental stressors, including dioxins, polycyclic aromatic hydrocarbons, and ultraviolet radiation, is the aryl hydrocarbon receptor (AHR). By regulating keratinocyte proliferation and differentiation, epidermal barrier function, melanogenesis, and immunity, a certain degree of AHR activity is critical to maintain skin integrity and to adapt to acute stress situations. In contrast, a chronic activation of cutaneous AHR signaling critically contributes to premature aging and the development of neoplasms by affecting metabolism, extracellular matrix remodeling, inflammation, pigmentation, DNA repair, and apoptosis. This article provides an overview of the detrimental effects associated with sustained AHR activity in chronically stressed skin and pinpoints AHR as a promising target for chemoprevention.

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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 Caucasian women with (n=29) and without (n=30) PCOS and related to metabolic features. PCBs were fractionated then analysed by high-resolution gas chromatography-unit resolution mass spectrometry. Results:. The control and PCOS groups were age and BMI matched (p=ns); insulin resistance was not different (HOMA 1.7±1.0 v 2±1.6, p=ns) but free androgen index was increased in PCOS (p<0.004). PCB-118, 138, 153 and 180 were found in all subjects, whilst fewer subjects showed PCB-28(15/59), PCB-52(4/59) or PCB-101(26/59). There was no difference for PCB-188,138,153 and 180 between controls and PCOS, but all correlated with increasing age (p<0.01) and decreasing estimated glomerular filtration rate (p<0.05); no correlations with BMI, HOMA, testosterone, TSH or T3 were found; however, PCB-118 (the only coplanar PCB detected) associated with an increased T4/T3 ratio (p<0.01). Conclusion. Despite PCBs being banned over a decade ago, PCBs were detected, but did not differ between age and BMI matched women with and without PCOS. Thyroid dysfunction may be only associated with toxic coplanar PCBs, such as PCB-118 that was associated with a higher T4/T3 ratio.

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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 females, this review will focus on the small number of studies performed in males that report an association of polychlorinated biphenyls with earlier sexual maturity rating and confirm subtle effects of lead, dioxins, and endosulfan on delaying pubertal onset and progression in boys. Recent studies have also demonstrated that EDC exposure may affect pubertal testosterone production without having a noticeable effect on sexual maturity rating. A limitation to understand the effects of EDCs in humans is the potential for confounding due to the long temporal lag from early-life exposures to adult outcomes. The complex interplay of multiple environmental exposures over time also complicates the interpretation of human studies. These studies have identified critical windows of vulnerability during development when exposures to EDCs alter critical pathways and affect postnatal reproductive health. Contemporaneous exposures can also disrupt the hypothalamic–pituitary–gonadal axis. This paper will review the normal process of puberty in males and summarize human data that suggest potential perturbations in pubertal onset and tempo with early-life exposures to EDCs.

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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 have suffered from 5 times more deaths from the corona virus infection than neighboring countries like Germany, Switzerland, Austria, and Denmark related to the size of their respective populations. There is a striking correlation between the level of environmental pollutants including pesticides, dioxins, and air pollution such as NO2 known to affect immune function and healthy metabolism with the rate of mortality in COVID-19 pandemic in these European countries. There is also a correlation with the use of chlorination of drinking water in these regions. In addition to the improvement of environmental protective programs, there are possibilities to lower the blood levels of these pollutants by therapeutic apheresis. Furthermore, therapeutic apheresis might be an effective method to improve metabolic inflammation, altered vascular perfusion, and neurodegeneration observed as long-term complications of COVID-19 disease.

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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 effects on the skin, metabolism (fever), the haematopoietic tissue, the respiratory system, the central and peripheral nervous system, the kidney and the gastrointestinal tract. Although PCP is not classified as a human carcinogen, some epidemiological observations suggest that exposure to chlorophenols in general and PCP solutions in particular may result in an increased risk for certain malignant disorders such as nasal carcinoma and soft tissue sarcoma. There is concern that contamination of PCP-solutions with products such as chlorodibenzo-p-dioxins is the real cause of this suspected carcinogenicity. No specific antidote exists for the treatment of (acute) PCP poisoning. The basis of the treatment of acute poisoning is intensive supportive care with prevention of dangerous rise in temperature. Use of PCP-based products as indoor wood preservatives poses an unacceptable risk to human health.

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