Academic literature on the topic 'Dioxins Metabolism'
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Journal articles on the topic "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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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.
Full textDissertations / Theses on the topic "Dioxins Metabolism"
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Furness, Sebastian George Barton. "Novel mechanisms for activation of the dioxin (Aryl-hydrocarbon) receptor /." Title page, table of contents and summary only, 2003. http://web4.library.adelaide.edu.au/theses/09PH/09phf988.pdf.
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Högberg, Pi. "Disruption of vitamin A metabolism by dioxin /." Stockholm, 2003. http://diss.kib.ki.se/2003/91-7349-608-1/.
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Shinkyo, Raku. "Structure-function analysis of mammalian cytochromes P450 involved in metabolism of dioxins." Kyoto University, 2006. http://hdl.handle.net/2433/144094.
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Kyoto University (京都大学)0048
新制・課程博士
博士(農学)
甲第12357号
農博第1538号
新制||農||923(附属図書館)
学位論文||H18||N4115(農学部図書室)
24193
UT51-2006-J349
京都大学大学院農学研究科食品生物科学専攻
(主査)教授 井上 國世, 教授 吉川 正明, 教授 村田 幸作
学位規則第4条第1項該当
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Hu, Keke. "Structure-activity relationships for the metabolism of polychlorinated dibenzo-p-dioxins and related compounds." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1999. http://www.collectionscanada.ca/obj/s4/f2/dsk2/ftp03/NQ35799.pdf.
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Murtomaa-Hautala, M. (Mari). "Species-specific effects of dioxin exposure on xenobiotic metabolism and hard tissue in voles." Doctoral thesis, Oulun yliopisto, 2012. http://urn.fi/urn:isbn:9789514297830.
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Abstract The evaluation of the effects and levels of contaminants in wildlife is an essential part of assessing risks for chemical exposure in the environment. Although the circumstances are not as controlled as in laboratory, wildlife studies offer the concept of environmental exposure in its entirety, with all the natural variation. In the present study, two wild vole species, bank vole (Myodes glareolus) and field vole (Microtus agrestis), were used in assessing environmental levels of dioxins. The effects of dioxin exposure on tooth and bone development were studied in order to determine whether they could be used as biomarkers for environmental exposure. Xenobiotic metabolism activity after dioxin exposure – both natural and experimental – was studied by quantifying selected cytochrome P-450 (CYP) enzymes. The results confirmed the fact that dioxins are ubiquitous in the environment, also in areas far from contaminant sources and human activity. The development of the third molar in bank vole was found to be a sensitive biomarker for dioxin exposure. The two vole species under study do not respond similarly to environmental concentrations of dioxins; there were significant differences in body burdens and activity levels of xenobiotic metabolizing enzymesTiivistelmä Haitallisten kemikaalien tason ja vaikutusten arviointi ympäristössä on olennainen osa kemikaalien riskin arviointia. Vaikka laboratoriossa olosuhteita kontrolloidaan ja tutkimukseen vaikuttava variaatio on paremmin hallittavissa, luonnonvaraisten lajien tutkiminen luo kokonaisvaltaisen ja todenmukaisen kuvan ympäristön kemikaalialtistuksesta kaikkine todellisine vaihteluineen. Tässä väitöskirjassa tarkastellaan kahden luonnonvaraisen pikkunisäkkään, metsämyyrän (Myodes glareolus) ja peltomyyrän (Microtus agrestis), käyttöä ympäristön kemikaalitason arvioinnissa. Pääpaino on dioksiinien kaltaisissa yhdisteissä. Työssä tutkitaan yhdisteiden kertymistä myyriin kahdessa ympäristössä: voimakkaasti dioksiineilla saastuneella maa-alueella sekä kaukana ihmistoiminnasta sijaitsevassa erämaassa. Herkiksi tiedettyjä vasteita – hampaiden ja luiden kehitystä – käytetään dioksiinialtistuksen indikaattoreina. Vierasainemetaboliasta vastaavien entsyymien (sytokromi P450 eli CYP) aktiivisuutta kartoitetaan molemmilla myyrälajeilla, jotta saadaan tietoa entsyymien indusoinnista luonnonvaraisilla myyrillä yleensä ja selvitetään havaittuja lajien välisiä eroja dioksiinivasteissa. Tulokset vahvistavat, että dioksiinit ovat laajalle levinneitä yhdisteitä, joita löytyy paitsi läheltä päästölähdettä myös kaukana ihmistoiminnasta olevilta alueilta. Metsämyyrällä kolmannen poskihampaan kehitys osoittautuu herkäksi dioksiinialtistuksen biomarkkeriksi. Samasta elinympäristöstä huolimatta tutkituista myyrälajeista mitatut dioksiinipitoisuudet eroavat huomattavasti toisistaan, samoin kuin vierasainemetaboliasta vastaavien entsyymien aktiivisuus ja niiden induktio TCDD-altistuksen jälkeen
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Labaronne, Emmanuel. "Impacts métaboliques d'un mélange faiblement dosé de polluants alimentaires dans un modèle murin : effets dépendants de l'âge, du sexe et du contexte nutritionnel." Thesis, Lyon, 2016. http://www.theses.fr/2016LYSE1204/document.
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Plusieurs travaux suggèrent l'implication des polluants de l'environnement dans l'épidémie d'obésité et l'incidence du diabète. Cependant, l'impact cumulé de cette myriade de polluants auxquels l'homme est exposé à faibles doses pendant toute sa vie n'a pas été totalement appréhendé.Au laboratoire, nous utilisons un modèle souris d'exposition chronique (toute la vie) à un mélange de polluants (TCDD, PCB153, DEHP et BPA) via leur ajout à une alimentation obésogène ou standard. Les doses des polluants sont ajustées de sorte à ce que l'exposition soit de l'ordre de la Dose Journalière Tolérable, supposée sans effet chez l'homme, pour chacun des 4 polluants.Nos résultats montrent que dans un contexte d'obésité induite par le régime et à l'âge adulte, l'exposition au mélange de polluants altère le métabolisme hépatique du cholestérol chez les mâles et aggrave l'intolérance au glucose chez les femelles. L'analyse du profil métabolique de femelles immatures nourries avec le régime obésogène indique que les effets des polluants sont liés au contexte hormonal et à l'activité oestrogéno-mimétique des polluants. Enfin, en condition de régime standard, nous observons une dyslipidémie chez les femelles adultes exposées au mélange, possiblement en lien avec la dérégulation génique dans le foie de plusieurs voies métaboliques dont le rythme circadien et le métabolisme du cholestérol. En revanche, les polluants n'ont pas d'effet obésogène.En conclusion, nos travaux démontrent que les polluants en mélange exercent un impact métabolique adverse chez la souris à des doses supposées sans effet individuellement, et ces effets sont dépendants du sexe de l'âge et du contexte alimentairePollutants are suspected to contribute to the etiology of obesity and related metabolic disorders but the current risk assessment does not take into account the cocktail effect resulting from the large amount of chemicals to which humans are exposed.We fed mice with high fat or standard diet with or without a mixture of food pollutants, either persistent pollutants (TCDD, PCB153) or short-lived pollutants (DEHP, BPA). Doses are adjusted resulting in mice exposure at the Tolerable Daily Intake dose range for each pollutant. Mice are chronically exposed from preconception to adult life.We demonstrated that a mixture of 4 pollutants triggers in the adult male offspring (12 weeks) an alteration of hepatic cholesterol metabolism. In females, there was a marked deterioration of glucose tolerance, which may be related to decreased hepatic estrogen signaling. The analyze of 7 week-old female mice, when they exhibit early signs of obesity and immature estrogen levels, shown that pollutant exposure alleviated HFSD-induced glucose intolerance, suggesting apparent biphasic effects of pollutants along with hormonal context. Then we compared hepatic signature of gene expressions from exposed non-obese or non exposed obese females and we highlight 4 main pathways that were targeted by both treatments and appeared to be affected by different but overlapping mechanisms. Plus, we showed that pollutants can markedly alter the circadian clock in the liver.Altogether, we emphasize that, pollutants presented in a mixture, have adverse metabolic effects at doses where they are supposed to be without any individual effect, and these effects depend on the gender, age and dietary context
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Arnoldsson, Kristina. "Polybrominated dibenzo-p-dioxins : Natural formation mechanisms and biota retention, maternal transfer, and effects." Doctoral thesis, Umeå universitet, Kemiska institutionen, 2012. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-50887.
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Polybrominated dibenzo-p-dioxins (PBDD) and dibenzofurans (PBDF) are a group of compounds of emerging interest as potential environmental stressors. Their structures as well as toxic responses are similar to the highly characterized toxicants polychlorinated dibenzo-p-dioxins. High levels of PBDDs have been found in algae, shellfish, and fish, also from remote areas in theBaltic Sea. This thesis presents studies on PBDD behavior in fish and offspring, and natural formation of PBDDs from naturally abundant phenolic precursors. The uptake, elimination, and maternal transfer of mono- to tetraBDD/Fs were investigated in an exposure study reported in Paper I. The effects of PBDDs in fish were examined in a dose-response study (Paper II). It was shown that fish can assimilate PBDD/Fs from their feed, although non-laterally substituted congeners were rapidly eliminated. Laterally substituted congeners were retained as was congeners without vicinal hydrogens to some extent. PBDD/Fs were transferred to eggs, and congeners that were rapidly eliminated in fish showed a higher transfer ratio to eggs. Exposure to the laterally substituted 2,3,7,8-TeBDD had significant effects on the health, gene expression and several reproduction end-points of zebrafish, even at the lowest dose applied. The geographical and temporal variations of PBDD in biota samples from the Baltic Seasuggest biogenic rather than anthropogenic origin. In Paper III, bromoperoxidase-mediated coupling of 2,4,6-tribromophenol yielded several PBDD congeners, some formed after rearrangement. The overall yield was low, but significantly higher at low temperature, and the product profile obtained was similar to congener profiles found in biota from the Swedish West Coast. In Paper IV, photochemically induced cyclization of hydroxylated polybrominated diphenyl ethers under natural conditions produced PBDDs at percentage yield. Rearranged products were not detected, and some abundant congeners do not seem to be formed this way. However, the product profile obtained was similar to congener profiles found in biota from the Baltic Proper. Since the PBDD congeners found in biota have a high turn-over in fish, the exposure must be high and continuous to yield the PBDD levels measured in wild fish. Thus, PBDDs must presumably be formed by common precursors in general processes, such as via enzymatic oxidations, UV-initiated reactions or a combination of both. The presented pathways for formation of PBDDs are both likely sensitive to changes in climatic conditions.
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Rosenzweig, Ella. "Exploring the role and the function of Aryl Hydrocarbon Receptor (AhR) and Aryl Hydrocarbon Nuclear Translocator (ARNT) in T cells." Thesis, University of Dundee, 2012. https://discovery.dundee.ac.uk/en/studentTheses/1d8657f4-b7b1-4508-a93f-76f21fa8d605.
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The Aryl Hydrocarbon Receptor (AhR) and the Aryl Hydrocarbon Nuclear Translocator (ARNT) play a role in mediating transcriptional responses to environmental pollutants, including the highly toxic compound 2,3,7,8-tetrachlorodibenzo -p-dioxin (TCDD) but also endogenous physiological ligands. More recent studies have also indicated that the AhR plays a role in the immune system notably in effector Th17 cells where it seems to be critical for the production of the IL-22 cytokine. It is known that AhR ligands such as dioxins can suppress CD8 T cell mediated antiviral immune responses but it is not known whether this reflects a direct role of the AhR in CD8 T cells.Accordingly, one objective of the present study was to explore AhR and ARNT expression in CD8 T cells. The initial strategy was to probe AhR and ARNT expression by western blot analysis. A second approach was to develop a mouse model that would fate mark single lymphocytes that have activated AhR signaling pathways. A third strategy was to examine the impact of deletion of AhR and ARNT on CD8 T-cell function.The data show that AhR and ARNT expression in CD8 T cells is limited to immune activated effector cells and these transcription factors are not expressed in naïve CD8 T cells. There are only low levels of AhR complexes in conventional CD8 positive cytotoxic T cells. To investigate AhR function at the single cell level we developed a mouse model to fate mark cells that have activated AhR signaling. In this model a mouse expressing Cre recombinase ‘knocked in’ to the CYP1A locus (CYP1A1Cre+/-) was backcrossed to the R26REYFP reporter mouse. In R26REYFP mice, a gene encoding EYFP is knocked into the ubiquitously expressed Rosa26 locus preceded by a loxP flanked stop sequence. CYP1A1 expression is controlled by AhR/ARNT complexes and the concept of our model was that cells that express AhR and ARNT complexes and are triggered with AhR ligands will express Cre recombinase and delete the loxP flanked stop sequence in the R26REYFP reporter locus and hence begin to express YFP.In vitro experiments demonstrated the validity of this AhR reporter model. The in vitro data reveal that expression of functional AhR/ARNT complexes occurs during Th17 and Tc17 cell differentiation but only a very low frequency of cytotoxic T cells activates the AhR. In vivo data found no evidence for AhR activation during T cell development in the thymus but show strong evidence for activation of AhR/ARNT signaling in innate lymphocytes in the gut. The ARNT transcription factor is highly expressed in cytotoxic T cells. These cells do not express functional AhR complexes, yet we considered that ARNT might play a role in CD8 T cell biology because of its ability to dimerise with the transcription factor Hif-1a. Our studies of T cells lacking ARNT expression revealed that in CD4 T cells the ARNT transcription factor regulates IL-17 and IL-22 production. In CD8 T cells we discovered that Hif-1a/ARNT signaling controls glycolysis in immune activated cells by sustaining expression of glucose transporters and multiple rate limiting glycolytic enzymes. ARNT was not required for CD8 T cell proliferation but was required for immune activated CD8 T cells to normally differentiate to express perforin and granzymes and to acquire the migratory program of effector T cells. Importantly, we discovered that Hif-1a/ARNT signaling is regulated by mTOR (mammalian target of rapamycin) thus revealing a fundamental mechanism linking nutrient sensing and transcriptional control of CD8 T-cell differentiation.
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Leblanc, Alix. "Effets d’un mélange de polluants organiques persistants sur le métabolisme hépatique." Thesis, Paris 5, 2014. http://www.theses.fr/2014PA05P629/document.
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Des études épidémiologiques ont montré que l’exposition à certains xénobiotiques est associée à une augmentation de la prévalence des maladies métaboliques. L’Homme est exposé à des mélanges de xénobiotiques de manière chronique et inévitable. Nous avons étudié les effets de l’interaction de deux xénobiotiques sur le métabolisme du foie, organe majeur de détoxification de l’organisme. Nous avons choisi deux perturbateurs endocriniens et polluants organiques persistants, qui activent des voies de signalisation différentes: la 2, 3, 7, 8 tétrachlorodibenzo-p-dioxine (TCDD), agissant via le récepteur aux hydrocarbures aromatiques (AhR), et l’α-endosulfan, un pesticide organochloré, qui peut agir via la voie du récepteur aux oestrogènes (ER) ou du récepteur X aux pregnanes (PXR). Notre objectif est de déterminer l’effet du mélange de ces polluants par rapport à chaque polluant isolé sur la régulation de certaines voies du métabolisme hépatique in vitro dans la lignée hépatocytaire humaine, HepaRG. Dans une première publication, une étude du transcriptome de cellules HepaRG différenciées a été effectuée. Ces cellules ont été exposées pendant 30 heures à 25nM de TCDD, 10μM d’α-endosulfan, ou au mélange. Nous avons observé que le mélange inhibe fortement l’expression de certains gènes impliqués dans le métabolisme glucidique et dans celui des alcools. Dans une seconde étude, nous avons donc étudié le mécanisme d’action du mélange sur le métabolisme glucidique. L’expression de deux gènes de la néoglucogenèse hépatique, le transporteur de glucose 2 (Glut2) et la glucose 6 phosphatase (G6Pc), est réduite de plus de 80% par le mélange. L’expression d’autres gènes du métabolisme glucidique (pyruvate kinase, glycogène synthase, glycogène phosphorylase, pyruvate déhydrogénase 2) est aussi diminuée, suggérant que le mélange peut affecter ce métabolisme de manière significative. De plus, la production de glucose diminue de 80% avec le mélange dans des conditions néoglucogéniques. En condition glycolytique, l’oxydation du glucose en CO2 diminue de 30% après 72 heures d’exposition au mélange. Un traitement à plus long terme (8 jours) avec des doses plus faibles des polluants (0.2 à 5nM de TCDD, 3μM d’α-endosulfan) diminue aussi l’expression de la G6Pc et de Glut2. Nous avons montré que la TCDD active bien la voie du AhR, et que le ER est impliqué dans l’action de l’α-endosulfan. Dans la troisième partie de cette thèse, nous avons étudié la régulation de plusieurs enzymes impliquées dans le métabolisme de l’alcool (alcool déshydrogénases, ADHs, cytochrome P450 2E1, CYP2E1) après l’activation du AhR. Les agonistes du AhR entrainent la diminution de l’expression des ARNm des ADH1, 4, 6 et du CYP2E1 et des protéines correspondantes. Nous avons montré que cette régulation utilise la voie génomique du AhR. De plus, cet effet est également observé après traitement de 8 jours par de faibles doses de TCDD. L’exposition chronique de l’Homme à de faibles doses de xénobiotiques en mélange pourrait affecter le métabolisme glucidique hépatique et contribuer, en partie, au développement du syndrome métaboliqueEpidemiological studies have shown that exposure to certain xenobiotics is associated with an increased prevalence of metabolic diseases. Humans are exposed to mixtures of xenobiotics in a chronic and inevitable way. We studied the effects of the interaction of two xenobiotics on metabolism in the liver, the major organ for detoxification in the body. We chose two endocrine disruptors and persistent organic pollutants which activate different signaling pathways: 2,3,7,8 tetrachlorodibenzo-p-dioxin (TCDD), which uses the AhR (Aryl hydrocarbon receptor) pathway, and α-endosulfan, an organochlorine pesticide, which acts via the PXR (pregnane X receptor) and/or the ER (estrogen receptor) pathway. Our aim was to determine the effects of this pollutant mixture, as compared to each pollutant alone, on the regulation in vitro of some hepatic metabolism pathways in the human hepatic cell line, HepaRG. In the first publication, a transcriptomic study of differentiated HepaRG cells was performed. The cells were exposed for 30h to 25nM TCDD, to 10 µM α-endosulfan or to the mixture. We observed that the mixture strongly inhibited the expression of some genes involved in the metabolism of glucose and alcohol. In the second study, we studied the mechanism of action of the mixture of pollutants on the metabolism of glucose. The expression of two genes involved in hepatic gluconeogenesis, glucose transporter 2 (GLUT2) and glucose-6-phosphatase (G6Pc), were reduced 80% by the mixture. The expression of other glucose metabolism genes (pyruvate kinase, glycogen synthase, glycogen phosphorylase, pyruvate dehydrogenase 2) also was decreased suggesting that the mixture might impact markedly carbohydrate metabolism. Furthermore, glucose production decreased 40% with the mixture under gluconeogenic conditions. Under glycolytic conditions, the oxidation of glucose into CO2 decreased 30% after 72h of exposure of the cells to the mixture. Long-term treatment (8 days) with lower doses (0.2 to 5 nM TCDD, 3 µM α-endosulfan) similarly decreased G6Pc and GLUT2 expression. We showed that TCDD activated the AhR pathway, and that ER was partly involved in the α-endosulfan effect. In the third part of this thesis, we studied the regulation of several enzymes involved in the metabolism of alcohol (alcohol dehydrogenase, ADH, cytochrome P450 2E1, CYP2E1) after activation of AhR. AhR agonists led to a decrease in the amounts of mRNAs for ADH1, 4, 6 and CYP2E1 and the corresponding proteins. We showed that this regulation uses the AhR genomic pathway. Furthermore, this effect was also observed after 8 days of treatment with lower doses of TCDD. Chronic exposure of individuals to low doses of xenobiotics in mixtures might significantly affect hepatic carbohydrate metabolism and be a contributing factor for the development of the metabolic syndrome
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Gadupudi, Gopi Srinivas. "PCB126-induced metabolic disruption: effects on liver metabolism and adipocyte development." Diss., University of Iowa, 2016. https://ir.uiowa.edu/etd/2208.
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Recently, persistent organic pollutants such as polychlorinated biphenyls (PCBs) were classified as “metabolic disruptors” for their suspected roles is altering metabolic and energy homeostasis through bioaccumulation in liver and adipose tissues. Among PCBs, a specific congener, 3,3',4,4',5-pentachlorobiphenyl (PCB126), is a potent arylhydrocarbon receptor (AhR) agonist and elicits toxicity similar to the classic dioxin, 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD). PCB126 levels found in human blood are particularly associated with diabetes and nonalcoholic fatty liver disease (NAFLD) in humans, however the mechanisms are unclear.
We hypothesized that the accumulation of PCB126 disrupts carbohydrate and lipid metabolism by altering the functions of liver and adipose tissues. Hence, our objective was to characterize PCB126 induced-metabolic disruption and the underlying molecular mechanisms that cause toxicity. Separate animal studies were performed using a rat model to understand the time- and dose-dependent effects after PCB126 administration. The chronology of PCB126 toxicity showed early decreases in serum glucose level at 9 h, worsened in a time-dependent way until the end of the study at 12 d. Lipid accumulation and the liver pathology also worsened over time between 3 d and 12 d post administration. These observed effects in the liver were also found to be dose-dependent. The decrease in serum glucose was a result of a decrease in the transcript levels of gluconeogenic and glycogenolytic enzymes, necessary for hepatic glucose production and hence the maintenance of steady glucose levels in the blood. Phosphoenolpyruvate carboxykinase (PEPCK-C), the rate limiting enzyme of gluconeogenesis, was found to be significantly decreased upon exposure to PCB126. The expression levels of peroxisome proliferator-activated receptor alpha (Pparα) and some of its targets involved in fatty acid oxidation were also found to be time and dose-dependently decreased upon exposure to PCB126. In an attempt to understand the molecular targets that may cause these dual effects on both gluconeogenic and fatty acid oxidation, we found that PCB126 significantly decreases phosphorylation of the cAMP response element-binding protein (CREB). CREB is a nuclear transcription factor that is activated in the liver through phosphorylation; to switch-on the transcription of enzymes that catalyze gluconeogenesis and fatty acid oxidation, in order to meet energy demands, especially during fasting.
Further, to understand the toxicity of PCB126 on adipose tissue, a human pre-adipocyte model that can be differentiated into mature adipocytes was used. In these studies, we found that exposure of preadipocytes to PCB126 resulted in a significant reduction in their ability to differentiate into adipocytes. This results in decreased lipid accumulation in the adipocyte. Reduction in the differentiation by PCB126 was associated with down regulation in transcript levels of a key adipocyte transcription factor, PPARγ and its transcriptional targets necessary for adipogenesis and adipocyte function. These inhibitory effects of PCB126 on the regulation of PPARγ and the initiation of adipogenesis were mediated through activation of AhR.
Overall, this work shows that PCB126 disrupts nutrient homeostasis through its effects on the function of target tissues; liver and adipose. PCB126 significantly alters the nutrient homeostasis through its effects on gluconeogenesis and fatty-acid oxidation necessary for glucose and energy regulation during fasting. In addition, PCB126 interrupts the storage functions of adipose tissue by inhibiting adipogenesis and thus disrupts lipid storage and distribution
Books on the topic "Dioxins Metabolism"
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Pohjanvirta, Raimo. The AH receptor in biology and toxicology. Hoboken, N.J: Wiley, 2011.
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NATO Advanced Study Institute on Carbon Dioxide: Chemical and Biochemical Uses as a Source of Carbon (1986 Pugnochiuso, Italy). Carbon dioxide as a source of carbon: Biochemical and chemical uses. Dordrecht: D. Reidel Pub. Co., 1987.
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The slender thread: Web of life, the story of carbon dioxide. Corpus Christi: Helix Press, 1985.
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McKinney, Aubrey R. The slender thread: Web of life, the story of carbon dioxide. Corpus Christi, Tex: Helix Press, 1995.
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Thoene, Barbara. Untersuchungen zur Aufnahme und Metabolisierung atmosphärischen Stickstoffdioxyds in oberindischen Organen der Fichte (Picea abies (L.) Karst.). Frankfurt/M: Wissenschafts-Verlag W. Maraun, 1991.
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W, Ludden Paul, Burris John E, and Burris Robert H. 1914-, eds. Nitrogen fixation and CO₂ metabolism: Proceedings of the Fourteenth Steenbock Symposium held 17-22 June 1984 at the University of Wisconsin--Madison, Madison, Wisconsin, U.S.A. New York: Elsevier, 1985.
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Ludden, P. W., and J. E. Burris. Nitrogen Fixation and Carbon Dioxide Metabolism. Elsevier, 1985.
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Nahas, G. Carbon Dioxide and Metabolic Regulations. Springer, 2011.
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Pohjanvirta, Raimo. AH Receptor in Biology and Toxicology. Wiley & Sons, Incorporated, John, 2011.
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Pohjanvirta, Raimo. AH Receptor in Biology and Toxicology. Wiley & Sons, Incorporated, John, 2011.
Find full textBook chapters on the topic "Dioxins Metabolism"
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Jaiswal, Prashant Kumar, and Jyotsana Gupta. "Metabolism of Dioxins and Dioxins-Like Compound, Its Regulation and Toxicological Pathways." In Environmental Microbiology and Biotechnology, 293–308. Singapore: Springer Singapore, 2020. http://dx.doi.org/10.1007/978-981-15-7493-1_14.
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Miller, Alexander L. "Carbon Dioxide Narcosis." In Cerebral Energy Metabolism and Metabolic Encephalopathy, 143–62. Boston, MA: Springer US, 1985. http://dx.doi.org/10.1007/978-1-4684-1209-3_6.
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Ranimol, G., C. B. Devipriya, and Swetha Sunkar. "Docking and Molecular Dynamics Simulation Studies for the Evaluation of Laccase Mediated Biodegradation of Triclosan." In Proceedings of the Conference BioSangam 2022: Emerging Trends in Biotechnology (BIOSANGAM 2022), 205–13. Dordrecht: Atlantis Press International BV, 2022. http://dx.doi.org/10.2991/978-94-6463-020-6_20.
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AbstractTriclosan (TCA) is an antibacterial and antimicrobial compound that is incorporated into toothpaste, soap, and liquid dishwasher. Continuous TCA exposure may contribute to the emergence of antibiotic-resistant bacteria in the microbiome. Triclosan also reacts to form dioxins, which bioaccumulate and are toxic to aquatic organisms, impedes the thyroid hormone metabolism of the human body. Laccases are multi copper-containing enzymes that can degrade the aromatic compounds and thus reduce their toxicity. To effectively degrade the compound, it is essential to understand the molecular function of the enzyme. Hence, a molecular docking study of laccase enzymes with Triclosan was done. The Tramates versicolor laccase structure was retrieved from PDB and ligand structure was taken from Pubchem. The binding mode and interaction of TCA and laccase were studied using Auto dock Vina software and the stability of the docked complex had been explored via Molecular Dynamics (MD) simulation study using Schrodinger Desmonde. The binding affinity score was found to be −6.5kcal/mol. The majority of the residues in RMSF were within the 2.5Å limit. The radius of gyration remained within the range from 21.7 to 22.1Å for Laccase – TCA complex throughout the 50 ns simulation. MD simulation results show that the enzyme complex remains stable all through the catalytic action.
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Karol, Paul J. "Respiration and Metabolism." In The Legacy of Carbon Dioxide, 153–64. Boca Raton : CRC Press, Taylor & Francis Group, 2019.: CRC Press, 2019. http://dx.doi.org/10.1201/9780429200649-15.
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Alscher, Ruth, Michael Franz, and C. W. Jeske. "Sulfur Dioxide and Chloroplast Metabolism." In Phytochemical Effects of Environmental Compounds, 1–28. Boston, MA: Springer US, 1987. http://dx.doi.org/10.1007/978-1-4613-1931-3_1.
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Sheoran, I. S., and Randhir Singh. "Carbon Dioxide Metabolism in Photosynthesis." In Concepts in Photobiology, 430–73. Dordrecht: Springer Netherlands, 1999. http://dx.doi.org/10.1007/978-94-011-4832-0_14.
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Kondo, Noriaki. "Uptake, Metabolism, and Detoxification of Sulfur Dioxide." In Air Pollution and Plant Biotechnology, 179–99. Tokyo: Springer Japan, 2002. http://dx.doi.org/10.1007/978-4-431-68388-9_9.
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Fuchs, Georg. "One-Carbon Metabolism of Anaerobic Bacteria: Challenge for Chemistry." In Enzymatic and Model Carboxylation and Reduction Reactions for Carbon Dioxide Utilization, 293–300. Dordrecht: Springer Netherlands, 1990. http://dx.doi.org/10.1007/978-94-009-0663-1_17.
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Yoneyama, Tadakatsu, Hak Y. Kim, Hiromichi Morikawa, and Hari S. Srivastava. "Metabolism and Detoxification of Nitrogen Dioxide and Ammonia in Plants." In Air Pollution and Plant Biotechnology, 221–34. Tokyo: Springer Japan, 2002. http://dx.doi.org/10.1007/978-4-431-68388-9_11.
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Li, Xin, Golam Jalal Ahammed, Lan Zhang, Peng Yan, Liping Zhang, and Wen-Yan Han. "Elevated Carbon Dioxide-Induced Perturbations in Metabolism of Tea Plants." In Stress Physiology of Tea in the Face of Climate Change, 135–55. Singapore: Springer Singapore, 2018. http://dx.doi.org/10.1007/978-981-13-2140-5_7.
Full textConference papers on the topic "Dioxins Metabolism"
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Gogol, Elina V., Guzel I. Gumerova, and Olga S. Egrova. "Approaches to Assessment and Hazard Identification of Dioxins." In Environmental Engineering. VGTU Technika, 2017. http://dx.doi.org/10.3846/enviro.2017.021.
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In the Russian practice in the framework of environmental regulation sanitary measurements to assess the toxicity of the objects of the environment, which are based on the determination of standardized components concentrations and comparing them with the limit value, are widely used. But this approach doesn’t allow assessing the degree of biological hazards for organisms. The biotesting method has been considered for assessing the safety of dioxin-like compounds. Dioxins can be formed out of control in the environment. Ultraviolet radiation accelerates the formation of dioxins, as it enhances the ability of a chemical reaction of chlorine. This phenomenon is well known in Russia, where the chlorination is a standard procedure of water treatment and disinfection of drinking water, and control of the content of chlorophenols is an optional procedure. Simulation of the formation of dioxins in the process of chlorination of water, containing phenolic compounds, was carried out. Process of dioxins transformation in living systems to more toxic metabolites has been described. Enzymes that are involved in detoxification of dioxins have been identified. According to the results of bioassay danger of water samples, containing dioxins, is underestimated, since it doesn’t take into account specific features of metabolism of dioxins in living organisms. Under the action of enzymes in the cells the less toxic compounds can be converted into the more toxic in terms of carcinogenicity and mutagenicity. The system of determination of the dioxin toxic equivalency factor doesn’t account for it. Thus, during determination of danger of xenobiotics in living organisms we should move away from the determination of acute toxicity and focus on the processes that are started by enzyme systems when a toxicant gets into cells of living organisms.
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Habran, S., Th Desaive, Ph Morimont, B. Lambermont, and P. C. Dauby. "Importance of metabolism variations in a model of extracorporeal carbon dioxide removal." In 2016 38th Annual International Conference of the IEEE Engineering in Medicine and Biology Society (EMBC). IEEE, 2016. http://dx.doi.org/10.1109/embc.2016.7591669.
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Albuquerque-Neto, Cyro, and Jurandir Itizo Yanagihara. "A Passive Model of the Heat, Oxygen and Carbon Dioxide Transport in the Human Body." In ASME 2009 International Mechanical Engineering Congress and Exposition. ASMEDC, 2009. http://dx.doi.org/10.1115/imece2009-11104.
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The aim of this work is the development of a mathematical model which integrates a model of the human respiratory system and a model of the human thermal system. Both models were previously developed at the same laboratory, based on classical works. The human body was divided in 15 segments: head, neck, trunk, arms, forearms, hands, thighs, legs and feet. Those segments have the form of a cylinder (circular cross-section) or a parallelogram (hands and feet) with the following tissue layers: muscle, fat, skin, bone, brain, lung, heart and viscera. Two different geometries are used to model the transport of mass and heat in the tissues. For the mass transfer, those layers are considered as tissue compartments. For the heat transfer, the body geometry is taken into account. Each segment contains an arterial and a venous compartment, representing the large vessels. The blood in the small vessels are considered together with the tissues. The gases are transported by the blood dissolved and chemically reacted. Metabolism takes place in the tissues, where oxygen is consumed generating carbon dioxide and heat. In the lungs, mass transfer happens by diffusion between an alveolar compartment and several pulmonary capillaries compartments. The skin exchanges heat with the environment by convection, radiation and evaporation. The differential transport equations were obtained by heat and mass balances. The discretization heat equations were obtained applying the finite volume method. The regulation mechanisms were considered as model inputs. The results show three different environment situations. It was concluded that the gas transport is most influenced by the temperature effects on the blood dissociation curves and the metabolism rise in a cold environment by shivering.
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Xia, Chunguang, and Nicholas Fang. "Enhanced Mass Transport Through Permeable Polymer Microcirculatory Networks." In ASME 2006 International Mechanical Engineering Congress and Exposition. ASMEDC, 2006. http://dx.doi.org/10.1115/imece2006-15408.
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One of the obstacles of culturing functioning vital tissues in vitro is to obtain a substantial biomass at a physiological cell density (>108cells/cm3). At this high density, the diffusion length of metabolites is limited to ~100um. As a matter of fact, in real tissue, almost all the cells are located within 100um distance from the capillaries [1]. Studies [2, 3] also confirmed that the cells in the artificial tissue cannot be properly cultured when they are further than 400um from the external nutrient source. Therefore, to culture three dimensional artificial tissue with substantial biomass, vascularization is necessary to enhance the metabolites transport. The short diffusion length of the metabolites requires high capillary density (>100/mm2) in vascularization. To meet this need, we have developed a novel high resolution and high speed 3D microfabrication technique, the projection microstereolithography[4] to explore microcirculatory networks with high density (>150/mm2). Using this technology we designed and fabricated the microreactors as shown in Figure 1. In our samples, 800um PEG microcapillaries with 20um inner radius and 40um outer radius with pitch of 96um are fabricated. Two rings as inlet and outlet are connected to external supply of culture medium. We designed the parameters of the vascularized microbioreactor based on the simulations of oxygen and carbon dioxide transport and metabolism in hepatocytes. As shown in Figure 2, the capillaries are arranged in a hexagonal way. According to the geometric symmetry, the final simulation domain is divided into 2 regions, the polymer capillary wall and the tissue. We assumed that a culture media with dissolved oxygen is pumped through the capillaries at 1.5mm/s rate and diffuses through the capillary wall, into the hepatocytes. The consumption of oxygen follows Michaelis-Menten kinetics [5, 6] and the metabolic rate of carbon dioxide is assumed to be proportional to that of oxygen by a fixed quotient (-0.81) which is addressed and studied by other groups [7]. The carbon dioxide diffuses into the capillaries and can be carried away through the flow of the culture medium. Our simulation indicates that the bottleneck of effective oxygen transport is the permeability of the polymer materials. The oxygen concentration drops off about 90% after diffusing through the capillary wall. It is predicted that the diffusion length at the inlet is 74um and 48um at the outlet; the rapid drop of carbon dioxide concentration also happens across the capillary wall. The predicted carbon dioxide concentration in the tissue is ~80nmol/cm3; this value is much smaller than the toxic value (100mmHg or 3umol/cm3) reported by David Gray and coworkers [8]. In Figure 2, we present the effect of the permeability of the capillary polymer materials on the diffusion length of oxygen and the concentration of carbon dioxide in the tissue. Our study indicates the existence of an optimal permeability for the capillary network, at which the overall diffusion length of oxygen is maximized. Interestingly, we also found a maximum concentration of carbon dioxide in the cultured tissue as the permeability of the polymer material changes. We attribute it to the competition between the tissue thickness and the permeability. Higher permeability increases the cultured tissue thickness, and also increases the ability of capillary to empty carbon dioxide. Not only is this model applicable for oxygen and carbon dioxide, but also for the transport of other metabolites. As an ongoing experimental effort, our fluorescent microscopy measurement validated the diffusion transport of fluorescent species from the capillary (Figure 3). Experiments are also in progress on the oxygen diffusion from the capillaries will cell cultures of high density on the PEG scaffold by introducing proper indicators. In summary, we have established a method to design and manufacture vascularized microcirculatory network to enhance the mass transport during the tissue culture. To ensure the effective nutrient delivery and wastes removal, our numerical simulation also confirms that it is essential to embed high density microcapillaries with optimal permeability.
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Ley, Obdulia, and Yildiz Bayazitoglu. "Effect of Physiological Parameters on the Temperature Distribution of a Layered Head Model." In ASME 2002 International Mechanical Engineering Congress and Exposition. ASMEDC, 2002. http://dx.doi.org/10.1115/imece2002-32044.
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Brain temperature control is important in clinical therapy, because moderate temperature reduction of brain temperature increases the survival rate after head trauma. A factor that affects the brain temperature distribution is the cerebral blood flow, which is controlled by autoregulatory mechanisms. To improve the existing thermal models of brain, we incorporate the effect of the temperature over the metabolic heat generation, and the regulatory processes that control the cerebral blood perfusion and depend on physiological parameters like, the mean arterial blood pressure, the partial pressure of oxygen, the partial pressure of carbon dioxide, and the cerebral metabolic rate of oxygen consumption. The introduction of these parameters in a thermal model gives information about how specific conditions, such as brain edema, hypoxia, hypercapnia, or hypotension, affect the temperature distribution within the brain. Existing biological thermal models of the human brain, assume constant blood perfusion, and neglect metabolic heat generation or consider it constant, which is a valid assumption for healthy tissue. But during sickness, trauma or under the effect of drugs like anesthetics, the metabolic activity and organ blood flow vary considerably, and such variations must be accounted for in order to achieve accurate thermal modeling. Our work, on a layered head model, shows that variations of the physiological parameters have profound effect on the temperature gradients within the head.
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Ito, Miu, and Yuichi Sugai. "Study on Enhanced Oil Recovery Using Microorganism Generating Foam in Presence of Nanobubbles." In SPE/IATMI Asia Pacific Oil & Gas Conference and Exhibition. SPE, 2021. http://dx.doi.org/10.2118/205671-ms.
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Abstract Both high cost and environmental load of surfactant are issues to be solved in foam EOR. Moreover, it is difficult to control the injection of surfactant and gas so that the foam is generated in only high permeable zones selectively in oil reservoir. The authors have found a foam generating microorganism and hit upon an idea of the microbial foam EOR which makes the microorganism do generating foam in oil reservoir. The mechanism of the microbial foam generation and culture condition suitable for the foam generation were studied in this study. A species of Pseudomonas aeruginosa was used as a foam producer in this study. It was cultured in the medium consisting of glucose and eight kinds of minerals at 30 °C and atmospheric pressure under anaerobic conditions. Because P. aeruginosa generally grows better under aerobic conditions, the microorganism was supplied with oxygen nanobubbles as the oxygen source. The carbon dioxide nanobubbles were also used as a comparison target in this study. The state of foam generation in the culture solution was observed during the cultivation. The surface tension, surfactant concentration, protein concentration, polysaccharides concentration and bacterial population of the culture solution were measured respectively. The foam was started to be generated by the microorganism after 2 days of cultivation and its volume became maximum after 3 days of cultivation. The foam generation was found in the culture solution which contained both oxygen nanobubbles and carbon dioxide nanobubbles whereas little foam was found in non-nanobubbles culture solution. The foam generation found in the culture solution containing carbon dioxide nanobubbles was more than that in the culture solution containing oxygen nanobubbles. Both gas and protein concentration increased along with the formation of the foam whereas surfactant and polysaccharides were not increased, therefore, the foam was assumed to be generated with gas and protein which were generated by P. aeruginosa. It was found that the carbon dioxide nanobubbles were positively charged in the culture medium whereas they were negatively charged in tap water through the measurement of zeta potential of nanobubbles, therefore, the carbon dioxide nanobubbles attracted cations in the culture medium and became positively charged. Positively charged carbon dioxide nanobubbles transported cations to the microbial cells of P. aeruginosa. Among cations in the culture medium, ferrous ions are essential for the protein generation of P. aeruginosa, therefore, the positively charged carbon dioxide nanobubbles attracted ferrous ions and transport them to the microbial cells, resulting the growth and metabolism of P. aeruginosa were activated. Those results suggest that the microbial foam EOR can be materialized by supplying the microorganism with carbon dioxide nanobubbles or ferrous ions.
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Zarin, A. S., Arup Lal Chakraborty, and Abhishek Upadhyay. "Detecting metabolic carbon dioxide using a tunable laser for non-invasive monitoring of growth of bacterial pathogens." In 2017 Conference on Lasers and Electro-Optics Europe & European Quantum Electronics Conference (CLEO/Europe-EQEC). IEEE, 2017. http://dx.doi.org/10.1109/cleoe-eqec.2017.8087202.
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Jacobs, A., and W. Everett. "A Fully Operational Pilot Plant for Eliminating Radioactive Oils Mixed With Chlorinated Solvents." In ASME 2011 14th International Conference on Environmental Remediation and Radioactive Waste Management. ASMEDC, 2011. http://dx.doi.org/10.1115/icem2011-59044.
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Disposal of organic liquid waste has become an increasing issue for many nuclear sites. Existing disposal solutions such as incineration or super critical water techniques are not compatible with wastes containing chlorinated solvents or fluorine owing to corrosion problems. As an example several hundred cubic meters of lubricating oils mixed with trichloroethylene (TCE) or perchloroethylene (PCE) are stockpiled on several French nuclear sites. For several years Dewdrops has been developing an original combination of mineralization processes for waste oils and solvents particularly well suited to the nuclear field. The patented technology relies on the alternation of chemical and biological oxidation mechanisms. The oxidized organic material predominately forms carbon dioxide, water and inorganic salts. This paper details the procedure and the results obtained for a particular case at the Tricastin nuclear site of Areva NC (South France). The organic waste used in this study was a 85/15 v/v ratio mix of lubricating oil and TCE. The pilot plant build upon the technology has a daily treatment capacity of approximately 10 liters. In the first step the TCE is mineralized by the photo Fenton reaction. Using hydrogen peroxide with an ultraviolet regenerated iron catalyst, TCE is transformed to carbon dioxide, water and hydrochloric acid. After neutralizing with caustic soda, the next step is a multi-stage biodegradation process to eliminate the remaining lubricating oil. Carefully selected microorganisms use the organic waste as an energy source for their metabolism. During oil biodegradation over 75% of the carbon is released as carbon dioxide while the remaining is incorporated into the biomass. The aqueous phase is continuously separated from the biomass using cross flow filters. The output aqueous phase is treated with ozone and ultraviolet light to eliminate the remaining organic compounds. The final effluent obtained is in conformance with European water standards and can be disposed by normal means. It can also be adjusted to local requirements. The radioactive elements and heavy metals present in these lubricating oils are trapped by the biomass. The excess of biomass is recovered by centrifugation and mineralized by catalytic ozonation technology. The result of the tests was a radioactive waste reduction factor of 15. The mineral residue is a concentrate of inorganic salts with traces of radioactive elements as well as heavy metals. The radioactive elements thus recovered can be consigned to an official repository.
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Pickering, Karen D., Eugene K. Ungar, Leticia M. Vega, and Melissa L. Campbell. "Fluid Mechanics and Biological Interaction in a Tubular Nitrifier Designed for Use in Space." In ASME 2000 International Mechanical Engineering Congress and Exposition. American Society of Mechanical Engineers, 2000. http://dx.doi.org/10.1115/imece2000-1420.
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Abstract Biological processes are currently being investigated for use in spacecraft wastewater treatment. In a biological wastewater processor, microorganisms are used to degrade organic and inorganic contaminants to carbon dioxide, water, and other metabolic products. One step in the process is nitrification, in which ammonium ions in the wastewater stream are converted to nitrate ions. Traditional reactor designs for nitrification, which include continuously stirred tank reactors and trickling filters, are unsuitable for use on spacecraft due to their reliance on gravity for aeration. A tubular reactor for aerobic nitrification in a microgravity environment has been developed to allow use of biological systems for wastewater treatment on spacecraft. The tubular reactor uses a 3.2 mm ID tube 305 m long with co-current air and wastewater flow. Aerobic microbes grow on the tube walls. Because of the small tube diameter and the high surface tension of the wastewater, the air/wastewater flow is gravity independent. Thus it is expected that the fluid flow and biological performance will be identical in Earth-normal gravity and in flight.
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Hossain, Md Shahadat, Shriram B. Pillapakkam, Bhavin Dalal, Ian S. Fischer, Nadine Aubry, and Pushpendra Singh. "Modeling of Blood Flow in the Human Brain." In ASME 2011 International Mechanical Engineering Congress and Exposition. ASMEDC, 2011. http://dx.doi.org/10.1115/imece2011-64525.
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Under normal conditions, Cerebral Blood Flow (CBF) is related to the metabolism of the cerebral tissue. Three factors that contribute significantly to the regulation of CBF include the carbon dioxide and hydrogen ion concentration, oxygen deficiency and the level of cerebral activity. These regulatory mechanisms ensure a constant CBF of 50 to 55 ml per 100g of brain per minute for mean arterial blood pressure between 60–180 mm Hg. Under severe conditions when the autoregulatory mechanism fails to compensate, sympathetic nervous system constricts the large and intermediate sized arteries and prevents very high pressure from ever reaching the smaller blood vessels, preventing the occurrence of vascular hemorrhage. Several invasive and non-invasive techniques such as pressure and thermoelectric effect sensors to Positron Emission Tomography (PET) and magnetic resonance imaging (MRI) based profusion techniques have been used to quantify CBF. However, the effects of the non-Newtonian properties of blood, i.e., shear thinning and viscoelasticity, can have a significant influence on the distribution of CBF in the human brain and are poorly understood. The aim of this work is to quantify the role played by the non-Newtonian nature of blood on CBF. We have developed mathematical models of CBF that use direct numerical simulations (DNS) for the individual capillaries along with the experimental data in a one-dimensional model to determine the flow rate and the methods for regulating CBF. The model also allows us to determine which regions of the brain would be affected more severely under these conditions.
Reports on the topic "Dioxins Metabolism"
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Eck, William S. Studies on Metabolism of 1,4-Dioxane. Fort Belvoir, VA: Defense Technical Information Center, March 2010. http://dx.doi.org/10.21236/ada528633.
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Johnson, K. M. Single-operator multiparameter metabolic analyzer (SOMMA) for total carbon dioxide (C{sub T}) with coulometric detection. Operator`s manual. Office of Scientific and Technical Information (OSTI), January 1992. http://dx.doi.org/10.2172/10194787.
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Wackett, Lawrence, Raphi Mandelbaum, and Michael Sadowsky. Bacterial Mineralization of Atrazine as a Model for Herbicide Biodegradation: Molecular and Applied Aspects. United States Department of Agriculture, January 1999. http://dx.doi.org/10.32747/1999.7695835.bard.
Full textAbstract:
Atrazine is a broadly used herbicide in agriculture and it was used here as a model to study the biodegradation of herbicides. The bacterium Pseudomonas sp. ADP metabolizes atrazine to carbon dioxide and ammonia and chloride. The genes encoding atrazine catabolism to cyanuric acid were cloned and expressed in Escherichia coli. The genes were designated atzA, atzB and atzC. Each gene was sequenced. The enzyme activities were characterized. AtzA is atrazine chlorohydrolase which takes atrazine to hydroxyatrizine. AtzB is hydroxyatrazine N-ethylaminohydrolase which produces N-isopropylammelide and N-ethylamine. AtzC is N-isopropylammelide N-isopropylaminohydrolase which produces cyanuric acid and N-isopropylamine. Each product was isolated and characterized to confirm their identity by chromatography and mass spectrometry. Sequence analysis indicated that each of the hydrolytic enzymes AtzA, AtzB and AtzC share identity which the aminohydrolase protein superfamily. Atrazine chlorohydrolase was purified to homogeneity. It was shown to have a kcat of 11 s-1 and a KM of 150 uM. It was shown to require a metal ion, either Fe(II), Mn(II) or Co(II), for activity. The atzA, atzB and atzC genes were shown to reside on a broad-host range plasmid in Pseudomonas sp. ADP. Six other recently isolated atrazine-degrading bacteria obtained from Europe and the United States contained homologs to the atz genes identified in Pseudomonas sp. ADP. The identity of the sequences were very high, being greater than 98% in all pairwise comparisons. This indicates that many atrazine-degrading bacteria worldwide metabolize atrazine via a pathway that proceeds through hydroxyatrazine, a metabolite which is non-phytotoxic and non-toxic to mammals. Enzymes were immobilized and used for degradation of atrazine in aqueous phases. The in-depth understanding of the genomics and biochemistry of the atrazine mineralization pathway enabled us to study factors affecting the prevalence of atrazine degradation in various agricultural soils under conservative and new agricultural practices. Moreover, Pseudomonas sp. ADP and/or its enzymes were added to atrazine-contaminated soils, aquifers and industrial wastewater to increase the rate and extent of atrazine biodegradation above that of untreated environments. Our studies enhance the ability to control the fate of regularly introduced pesticides in agriculture, or to reduce the environmental impact of unintentional releases.