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Relevant bibliographies by topics / Biochemical toxicology of PCBs

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Academic literature on the topic 'Biochemical toxicology of PCBs'

Author: Grafiati

Published: 4 June 2021

Last updated: 1 February 2022

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Journal articles on the topic "Biochemical toxicology of PCBs"

1

Safe, Stephen H. "Polychlorinated Biphenyls (PCBs): Environmental Impact, Biochemical and Toxic Responses, and Implications for Risk Assessment." Critical Reviews in Toxicology 24, no. 2 (January 1994): 87–149. http://dx.doi.org/10.3109/10408449409049308.

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Battershill, J. "To TEF or not to TEF? That is the question." Human & Experimental Toxicology 13, no. 8 (August 1994): 576–77. http://dx.doi.org/10.1177/096032719401300814.

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Commercial polychlorinated biphenyls (PCBs) and environmental extracts contain complex mixtures of congeners that can be unequivocally identified and quantitated. Some PCB mixtures elicit a spectrum of biochemical and toxic responses in humans and laboratory animals and many of these effects resemble those caused by 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) and related halogenated aromatic hydrocarbons, which act through the aryl hydrocarbon (Ah)-receptor signal transduction pathway. Structure-activity relationships developed for PCB congeners and metabolites have demonstrated that several structural classes for compounds exhibit diverse biochemical and toxic responses. Structure-toxicity studies suggest that the coplanar PCBs, namely, 3,3',4,4'-tetrachlorobiphenyl (tetraCB). 3,3',4,4',5-pentaCB, 3,3',4,4',5,5'hexaCB, and their monoortho analogs are AH-receptor agonists and contribute significantly to the toxicity of the PCB mixtures. Previous studies with TCDD and structurally related compounds have utilized a toxic equivalency factor (TEF) approach for the hazard and risk assessment of polychlorinated dibenzo-p dioxin (PCDD) and polychlorinated dibenzofuran (PCDF) congeners in which the TCDD or toxic TEQ = Σ([PCDFi X TEFi]n) + Σ([PCDDi x TEFi] n) equivalent (TEQ) of a mixture is related to the TEFs and concentrations of the individual (i) congeners as indicated in the equation (note: n = the number of congeners). Based on the results of quantitative structure-activity studies, the following TEF values have been estimated by making use of the data available for the coplanar and mono-ortho coplanar PCBs: 3,3',4,4'5-pentaCB,0.1; 3,3',4,4',5,5'-hexaCB,0.05 ; 3,3',4,4'-tetraCB,0.01; 2,3,3',4,4'-pentaCB,0.001 ; 2,3,4,4',5-pentaCB, 0.0001; 2,3,3',4,4',5-hexaCB,0.0003 ; 2,3,3',4,4',5'-hexaCB,0.0003; 2',3,4, 4',5-pentaCB,0.00005; and 2,3,4,4',5-pentaCB, 0.0002. Application of the TEF approach for the risk assessment of PCBs must be used with considerable caution. Analysis of the results of laboratory animal and wildlife studies suggests that the predictive value of TEQs for PCBs may be both species-and response-dependent because both additive and non-additive (antagonistic) interactions have been observed with PCB mixtures. In the latter case, the TEF approach would significantly overestimate the toxicity of a PCB mixture. Analysis of the rodent carcinogenicity data for assessment of PCB mixtures that uses cancer as the endpoint cannot solely utilize a TEF approach and requires more quantitative information on the individual congeners contributing to the tumor-promoter activity of PCB mixtures.

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Foerster, Claudia, Liliana Zúñiga-Venegas, Pedro Enríquez, Jacqueline Rojas, Claudia Zamora, Ximena Muñoz, Floria Pancetti, et al. "Levels of Polychlorinated Dibenzo-p-Dioxins/Furans (PCDD/Fs) and Dioxin-Like Polychlorinated Biphenyls (DL-PCBs) in Human Breast Milk in Chile: A Pilot Study." International Journal of Environmental Research and Public Health 18, no. 9 (April 30, 2021): 4825. http://dx.doi.org/10.3390/ijerph18094825.

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Persistent organic pollutants (POPs) are organic compounds that resist biochemical degradation, moving long distances across the atmosphere before deposition occurs. Our goal was to provide up-to-date data on the levels of polychlorinated dibenzo-p-dioxins/furans (PCDD/Fs) and dioxin-like polychlorinated biphenyls (DL-PCBs) in breast milk from Chilean women and to estimate the exposure of infants due to breast milk consumption. In Chile, we conducted a cross-sectional study based on methodologies proposed by the WHO, with a sample of 30 women recruited from three defined areas: 10 from the Arica Region (urban; Arica and Parinacota Region), 10 from Coltauco (rural; O’Higgins Region), and 10 from Molina (40% rural; Maule Region). High-resolution gas chromatography coupled with high-resolution mass spectrometry (HRGC/HRMS) was performed on pooled samples from each area. We calculated equivalent toxic concentrations (WHO-TEQ) based on the current WHO Toxic Equivalency Factors (TEF). The minimum and maximum values of ∑ PCDDs/Fs + DL-PCBs-TEQ were 4.317 pg TEQ/g fat in Coltauco and 6.31 pg TEQ/g fat in Arica. Molina had a total TEQ of 5.50 pg TEQ/g fat. The contribution of PCDD/Fs was approximately five-fold higher than that of DL-PCBs. The Estimated Daily Intake (EDI) of ∑ PCDDs/Fs + DL-PCBs based on the three pooled samples ranged between 6.71 and 26.28 pg TEQ/kg body weight (bw)/day, with a mean intake of 16.11 (±6.71) pg TEQ/kg bw/day in breastfed children from 0 to 24 months old. These levels were lower than those reported in international studies. Despite the fact that the observed levels were low compared to those in most industrialized countries, the detection of a variety of POPs in breast milk from Chilean women indicates the need for follow-up studies to determine whether such exposures during childhood could represent a health risk in adulthood.

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Sher, Ellen S., Xiao Ming Xu, Perrie M. Adams, Cheryl M. Craft, and Stuart A. Stein. "The Effects of Thyroid Hormone Level and Action in Developing Brain: Are These Targets for the Actions of Polychlorinated Biphenyls and Dioxins?" Toxicology and Industrial Health 14, no. 1-2 (January 1998): 121–58. http://dx.doi.org/10.1177/074823379801400110.

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Alterations in thyroid hormone level or responsivity to thyroid hormone have significant neurologic sequelae throughout the life cycle. Duringfetal and early neonatal periods, disorders of thyroid hormone may lead to the development of motor and cognitive disorders. During childhood and adult life, thyroid hormone is required for neuronal maintenance as well as normal metabolic function. Those with an underlying disorder of thyroid hormone homeostasis or mitochondrial function may be at greater risk for developing cognitive, motor, or metabolic dysfunction upon exposure to substances which alter thyroid hormone economy. Polychlorinated biphenyls (PCBs) and dioxins have been argued to interfere with thyroid hormone action and thus may affect the developing and mature brain. Animal models provide useful tools for studying the effects of thyroid hormone disorders and the effects of environmental endocrine disruptors. The congenitally hypothyroid, hyt/hyt, mouse exhibits abnormalities in both the cognitive and motor systems. In this mouse and other animal models of thyroid hormone disorders, delayed somatic and reflexive development are noted, as are permanent deficits in hearing and locomotor and adaptive motor behavior. This animal's behavioral abnormalities are predicated on anatomic abnormalities in the nervous system. In turn, these abnormalities are correlated with differences in neuronal structural proteins. In normal mice, the expression of mRNAs coding for these proteins occurs temporally with the onset of autonomous thyroid hormone production. The hyt/hyt mouse has a mutation in the thyroid stimulating hormone receptor (TSHr) gene which renders it incapable of transducing the TSH signal in the thyrocyte to produce thyroid hormone. Some behavioral and possibly some biochemical abnormalities in mice exposed to PCBs are similar to those seen in the hyt/hyt mouse. In addition to direct effects on brain development and neuronal maintenance, thyroid hormone is necessary for maintaining metabolic functioning through its influence on mitochondria. Because the brain is particularly sensitive to inadequate energy generation, disorders of thyroid hormone economy also indirectly impair brain functioning. Alterations in thyroid hormone level result in differing expression of mitochondrial genes. Mutations in these mitochondrial genes lead to well-recognized syndromes of encephalomyopathy, myopathy, and multisystem disorder. Hence, PCBs and dioxins, by possibly altering the thyroid hormone milieu, may alter thefunctioning of mitochondria in the generation of adenosine triphosphate (ATP). The use of animal models of thyroid hormone deficiency for behavioral, anatomic, histologic, and molecular comparison will help elucidate the mechanisms of action of these putative endocrine-disrupting compounds. The study of thyroid hormone disorders provides a template for relating thyroid hormone mediated effects on the brain to these compounds.

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Ujházy, Eduard, Mojmír Mach, Jana Navarová, Ingrid Brucknerová, and Michal Dubovický. "Teratology – past, present and future." Interdisciplinary Toxicology 5, no. 4 (December 1, 2012): 163–68. http://dx.doi.org/10.2478/v10102-012-0027-0.

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ABSTRACT Teratology is the science that studies the causes, mechanisms, and patterns of abnormal development. The authors present an updated overview of the most important milestones and stages of the development of modern teratology. Development of knowledge and society led to the recognition that causes of congenital developmental disorders (CDDs) might be caused by various mechanical effects, foetal diseases, and retarded or arrested development of the embryo and foetus. Based on the analysis of the historical development of hypotheses and theories representing a decisive contribution to this field, we present a survey of the six Wilson´s fundamental principles of teratology. The aim of observing these principles is to get insight into developmental relations and to understand mechanisms of action on the level of cell populations (elementary morphogenetic processes), tissues and organs. It is important to realise that any negative intervention into the normal course of these processes, either on genetic or non-genetic basis, inevitably leads to a sequence of subsequent changes resulting in CDDs. Moreover, the classical toxicologic monotonic doseresponse paradigm recently has been challenged by the so-called “low dose-hypothesis”, particularly in the case of endocrine active substances. These include some pesticides, dioxins, polychlorobiphenyls (PCBs), and bisphenol A. Despite modern approaches of molecular biology and genetics, along with top diagnostic techniques, we are still not able to identify the actual cause in more than 65 to 70% of all congenital defects classified as having an unknown etiology. Today CDDs include any birth defect, either morphological, biochemical, or behavioural.

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van den Berg, Martin, Bart L. H. J. Craane, Theo Sinnige, Sijmen van Mourik, Sjoerd Dirksen, Theo Boudewijn, Marten van der Gaag, Ineke J. Lutke-Schipholt, Bert Spenkelink, and Abraham Brouwer. "BIOCHEMICAL AND TOXIC EFFECTS OF POLYCHLORINATED BIPHENYLS (PCBs), DIBENZO-p-DIOXINS (PCDDs) AND DIBENZOFURANS (PCDFs) IN THE CORMORANT (PHALACROCORAX CARBO) AFTER IN OVO EXPOSURE." Environmental Toxicology and Chemistry 13, no. 5 (1994): 803. http://dx.doi.org/10.1897/1552-8618(1994)13[803:bateop]2.0.co;2.

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Van Den Berg, Martin, Bart L. H. J. Craane, Theo Sinnige, Sijmen VanMourik, Marten Van Der Gaag, Ineke J. Lutke-Schipholt, Bert Spenkelink, Abraham Brouwer, Sjoerd Dirksen, and Theo Boudewun. "Biochemical and toxic effects of polychlorinated biphenyls (PCBs), dibenzo-P-dioxins (PCDDs) and dibenzofurans (PCDFs) in the cormorant (phalacrocorax carbo) after in ovo exposure." Environmental Toxicology and Chemistry 13, no. 5 (May 1994): 803–16. http://dx.doi.org/10.1002/etc.5620130516.

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Cutler, David. "PCBs on a hook." Trends in Pharmacological Sciences 22, no. 8 (August 2001): 401–2. http://dx.doi.org/10.1016/s0165-6147(00)01782-x.

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Tan, Y. "Ortho-Substituted PCBs Kill Thymocytes." Toxicological Sciences 76, no. 2 (November 4, 2003): 328–37. http://dx.doi.org/10.1093/toxsci/kfg233.

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Fossi, Cristina, Claudio Leonzio, and Silvano Focardi. "Biochemical and physiological responses in gobiidae experimentally exposed to PCBs." Marine Environmental Research 24, no. 1-4 (January 1988): 113. http://dx.doi.org/10.1016/0141-1136(88)90268-1.

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Dissertations / Theses on the topic "Biochemical toxicology of PCBs"

1

Bazara, Salem Mohammed. "Biochemical studies on the toxicity and carcinogenicity of PCBs and related compounds." Thesis, Brunel University, 1988. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.235935.

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Hoffman, Jessie Baldwin. "PCB DISRUPTION OF GUT AND HOST HEALTH: IMPLICATIONS OF PREBIOTIC NUTRITIONAL INTERVENTION." UKnowledge, 2018. https://uknowledge.uky.edu/pharmacol_etds/25.

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Exposure to environmental pollutants poses numerous risk factors for human health, including increasing incidence of cardiovascular disease and diabetes. Persistent organic pollutants, such as polychlorinated biphenyls (PCBs) have been strongly linked to the development of these chronic inflammatory diseases and the primary route of exposure is through consumption of contaminated food products. Thus, the gastrointestinal tract is susceptible to the greatest levels of these pollutants and is an important facet to study. The first two hypotheses of this dissertation tested that exposure to PCBs disrupts gut microbiota directly (in vitro) and within a whole body system. PCB exposure disrupted microbial metabolism and production of metabolites (i.e. short chain fatty acids) in vitro. These disruptions in microbial populations were consistent in our mouse model of cardiometabolic disease, where we observed reductions in microbial diversity, an increase in the putative pro-inflammatory ratio of Firmicutes to Bacteroidetes, and reductions in beneficial microbial populations in exposed mice. Furthermore, observed greater inflammation was observed both within the intestines and peripherally in PCB exposed mice as well as disruptions in circulating markers associated with glucose homeostasis. Nutritional interventions high in prebiotic dietary fiber such as inulin may be able to attenuate the toxic effects of pollutant exposure. To test the hypothesis that consumption of the prebiotic inulin can decrease PCB-induced disruption in gut microbial and metabolic homeostasis, LDLr-\- mice were fed a diet containing inulin and exposed to PCB 126. Mice fed an inulin-containing diet and exposed to PCBs exhibited improved glucose tolerance, lower hepatic inflammation and steatosis, and distinct differences in gut microbial populations. Overall, these data suggests that nutritional intervention, specifically prebiotic consumption, may reduce pollutant-induced disease risk.

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Wangpradit, Orarat. "Prostaglandin H synthase catalyzes the oxidation of 4-chlorobiphenyl metabolites, and the in vivo effects on prostaglandin production." Diss., University of Iowa, 2011. https://ir.uiowa.edu/etd/1101.

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Polychlorinated biphenyls (PCBs) exert a broad range of toxicity via both parent compounds and their metabolites. Our previous study showed that hydroquinone (H2Q) metabolites of PCBs act as cosubstrates for prostaglandin H synthase (PGHS), and are oxidized by this enzyme to corresponding quinones (Q). The goal of this thesis is to illuminate the PGHS-mediated toxicity of lower chlorinated PCBs. It is hypothesized that PGHS catalyzes two sequential one-electron oxidations of PCB-H2Q to semiquinone (SQ), and Q that interact with biomolecules, such as amino acids, glutathione (GSH), protein, and DNA. In addition, the oxidation of H2Q by PGHS results in an elevation of downstream prostaglandin (PG) production in vivo. Employing 4-chlorobiphenyl-2f,5f-hydroquinone (4-CB-2f,5f-H2Q) as a model compound, I found that PGHS-2 catalyzes the one-electron oxidation of 4-CB-2f,5f-H2Q to SQ. An unusual electronically distorted SQ spectrum was observed as a result of the mixture of two different SQ species, a quartet and a doublet. Fate of 4-CB-2f,5f-SQ and/or Q in the presence of biomolecules was further investigated in the next study. 4-CB-2f,5f-SQ/Q reacts readily with the thiol-containing molecules, such as cysteine, and GSH. Oligonucleotides, and DNA did not form a covalent adduct with 4-CB-2f,5f-SQ but preferably stabilized 4-CB-2f,5f-SQ by pi-stacking interaction under the assay conditions. The in vivo study of downstream PG production in rats treated with 4-CB-2f,5f-H2Q revealed that PGE2 was significantly elevated in ratsf kidneys at 24 h post intratracheal instillation. The increased PGE2 production was correlated with an elevation of alveolar macrophages. These findings suggest two possible mechanisms of enhanced PGE2 production: i) 4-CB-2f,5f-H2Q as a cosubstrate for PGHS in kidney, and 2) release of cytokines from macrophages, leading to stimulation of PGE2 production in other tissues but released and accumulated in kidney for excretion. In summary, the toxicity of lower chlorinated PCBs metabolites is potentially mediated by PGHS. Quinones generated from the PGHS metabolic pathway covalently bind to GSH resulting in GSH depletion, and oxidative stress. The intercalation or pi-stacking of SQ in DNA may be implicated in genotoxicity as a result of the change in DNA structure.

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Rodriguez, Grau Jorge Luis. "Suppression of Immune Functions by PCBs in the Earthworm Lumbricus terrestris." Thesis, University of North Texas, 1989. https://digital.library.unt.edu/ark:/67531/metadc798391/.

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This research is part of an effort to develop non-mammalian surrogate immunoessays with the earth worm Lumbricus terrestris to assess immunotoxic potential of xenobiotics to mammals. The objective was to determine if earthworm immunoessays, namely E- and S- rosette formation and phagocytosis, are sensitive to a known mammalian immunotoxin, the PCB Arclor 1254. Results are presented in terms of PCB exposure and tissue concentrations during uptake/depuration.

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Enayah, Sabah Hassain. "Evaluation of alterations in dopamine and neuro-toxicity caused by co-exposure to lead (Pb) and polychlorinated biphenyls (PCBs)." Diss., University of Iowa, 2016. https://ir.uiowa.edu/etd/2072.

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Polychlorinated biphenyls (PCBs) are synthetic organic compounds that resist natural breakdown in the environment. Various toxic metals are found naturally in the earth and may become concentrated as a result a human activity. PCBs and toxic metals are a major public health concern due to human exposure from both natural and anthropogenic sources. Humans may be exposed to these chemicals from occupational sources, ingestion through food, drinking water and some medications. The main risk arising from environmental pollution by toxic metals and PCBS is damage to the nervous system. This thesis set out to answer two questions 1) does co-exposure to toxic metals and PCBs happen from occupational sources since these chemicals are present in various building materials? 2) Does co-exposure to Pb and the most abundant and neurotoxic PCBs (such as PCB153 or PCB95) generate more toxicity on neurons as compared to exposure to a single toxicant? To investigate whether co-exposure occurs from occupational sources, toxic metals and PCB (in progress) levels of 84 construction workers in eastern Iowa were assessed. Levels of DNA damage and antioxidant proteins associated with these exposures were also evaluated. The results revealed a wide range of Pb, Cd, and Hg levels in construction workers. Levels of DNA damage and levels of 8-Oxo-dG in these workers were influenced by whether they handled fluorescent light ballasts, whether they ate fish and whether they wore protective masks. To answer the second question a PC12 cell line was used, a well-known model for dopaminergic (DA) neurons, to study the effect of single and co-exposure on cell viability, DA level, DA metabolism, DA synthesis and packaging enzyme expression and antioxidant enzyme expression. The results illustrate that effects of single exposure to Pb, PCB153 and PCB95 and the combination of Pb and PCB153 or PCB95 following 12 and 24h exposure are variable and the effects are based on different mechanisms. Likewise, PCB153 and PCB95 which are both non-dioxin like PCBs were found to have different effects on PC12 cells based on the structure of the congener. This thesis demonstrates for the first time that PCB153 or PCB95 synergistically increase Pb toxicity to neurons, however, more research is needed to explore the interactions and the mechanisms which are involved in the influence of Pb in the presence of PCB.

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Duncan, Ian W. "Biochemical effects of polychlorinated biphenyls with reference to transfer in breast milk." Thesis, University of Bath, 1988. https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.383251.

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Coleman, M. D. "The biochemical pharmacology and toxicology of anti-parasitic agents." Thesis, Aston University, 2004. http://publications.aston.ac.uk/21356/.

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Salomon, Beltran Marisa Genevive. "Novel tools for targeting PCBs and PCB metabolites using ssDNA aptamers." Thesis, University of Iowa, 2016. https://ir.uiowa.edu/etd/2269.

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Polychlorinated biphenyls (PCBs) are persistent environmental chemicals. Mono-hydroxylated polychlorinated biphenyls (OH-PCBs) are PCB metabolites found commonly in human blood, environmental water and sediment samples. Detection of small amounts of PCBs and their OH-PCB metabolites in biological matrices from epidemiological and laboratory studies remains a challenge. The application of aptamers is studied as a means to identify and quantify PCBs and OH-PCBs. Aptamers are single stranded short oligonucleotides that arrange into unique shape of three-dimensional structures when binding to their target. Like antibodies they have high affinity and specificity for their specific target. The hypothesis is that aptamers can identify PCBs and PCB metabolites in environmental and biological samples. To test this hypothesis, three different OH-PCBs, 4’-OH-PCB3, 4-OH-PCB72 and 2-OH-PCB106 along with 4-OH-biphenyl as a control, were covalently attached to beads with carboxylic acid groups on their surface. Several methods were explored to characterize covalent binding of OH-PCBs to the beads: FTIR-spectroscopy, Dynamic Light Scattering (DLS) and Zeta-Potential (ZP) measurements. The beads were then used in in vitro assays to test binding of two different aptamers specific to OH-PCBs. In this study, these aptamers were tested for the ability to distinguish structurally different OH-PCB congeners and other environmental pollutants. In future studies, aptamers can be selected for a PCB metabolite of interest, 4’-OH-PCB3, via a modified form of Systemic Evolution of Ligands by Exponential Enrichment (SELEX). Single stranded DNA (ssDNA) aptamers generated will be applied as a biosensor for the detection and quantification of traces of 4’-OH-PCB3.

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Li, Miao. "Protein adducts and crosslinking by reactive metabolites of polychlorinated biphenyls (PCBs)." Diss., University of Iowa, 2015. https://ir.uiowa.edu/etd/1984.

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Polychlorinated biphenyls (PCBs) are the persistent environmental pollutants with the continuous concerns over adverse human health effects. As semi-volatile compounds, PCBs were found in indoor and outdoor air. The observation of high levels of airborne PCBs in old school buildings raised the concerns of inhalation exposure and toxicity of PCBs. Lower chlorinated PCBs (LC-PCBs), major components of airborne PCBs, are subject to biotranformation. In vitro and in vivo studies revealed that reactive metabolites of LC-PCBs formed covalent adducts on DNA and proteins. The hypothesis of the project is that the reactive metabolites of LC-PCBs are able to form adducts on proteins or even protein crosslinks, and the formation of protein adducts and crosslinks causes the dysfunction of the target proteins. In addition, the objectives of the project are also to identify protein targets by PCB metabolites, which may be related to the mechanism of toxicity of LC-PCBs. The alkaline permethylation (AP) was established and optimized to identify and measure the protein adducts from LC-PCB metabolites. The AP method evidenced PCB metabolites formed protein adducts through the sulfhydryl groups and also one molecule of PCB quinoid metabolites was able to bind to more than one protein. Application of cytochrome c as the model protein revealed PCB quinoid metabolites also formed adducts on lysine and glutamic acid. The adduct formation and crosslinks caused the dysfunction of cytochrome c. In addition, the quinone protein adducts still kept the ability for redox reactions, which may lead to unexpected toxicity. The SILAC method was applied to identify the target proteins in the samples of in vitro proteome incubation. The instability of PCB quinone protein adducts was found by further reaction of quinone protein adducts. This may be the reason why cysteine-PCB quinone adducts were not frequently identified by proteomics method. The further understanding of protein adducts by reactive PCB metabolites helps to identify the target proteins, and ultimately reveal the role of protein adducts impacting on human health.

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Xin, Xing. "Effects of polychlorinated biphenyls (PCBs) on telomere maintenance in hematopoietic stem cells and progenitor cells." Diss., University of Iowa, 2015. https://ir.uiowa.edu/etd/2026.

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Polychlorinated biphenyls (PCBs) are synthetic persistent organic compounds that are known to be carcinogenic to humans. Changes in telomerase activity and telomere length are hallmarks of aging and carcinogenesis. Retention of telomerase activity and long telomeres are key characteristics of stem cells and progenitor cells. I hypothesize that PCBs modulate telomerase activity and telomeres of hematopoietic stem cells and progenitor cells via interference of gene regulation and potentially disrupt cell differentiation. To investigate this possibility, I used progenitor-like cells, human promyelocytic leukemia cells (HL-60), and stem cells from rat bone marrow. I show that PCB126 and PCB153 display toxic effects on telomerase activity, telomere length and their related gene expression in progenitor-like HL-60 cells, but they did not exert much effect on differentiation. Further, an in vivo/in vitro study using rat bone marrow cells shows that PCB126-induced hematotoxicity, evidenced by reduction in telomerase activity and TERT gene expression, an increase of the differentiation and a change in the differentiation direction towards granulocytes, which indicate an effect on stem cell function. I also show that the most potent dioxin-like congener, PCB126, regulates hTERT gene expression by activation of the AhR pathway. Both AhR and ARNT work together as a repressor of hTERT transcription. This research improves our understanding of mechanisms of PCB126 and PCB153 toxicity on hematopoietic stem cells and progenitor cells, which will ultimately have significant implications for human health.

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Books on the topic "Biochemical toxicology of PCBs"

1

Principles of biochemical toxicology. 2nd ed. London: Taylor & Francis, 1991.

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Timbrell, John A. Principles of biochemical toxicology. London: Taylor & Francis, 1985.

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Timbrell, John A. Principles of biochemical toxicology. 4th ed. New York: Informa Healthcare USA, 2008.

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Principles of biochemical toxicology. 3rd ed. London: Taylor & Francis, 2000.

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Principles of biochemical toxicology. 3rd ed. London: Taylor & Francis, 2000.

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Smart, Robert C., and Ernest Hodgson, eds. Molecular and Biochemical Toxicology. Hoboken, NJ, USA: John Wiley & Sons, Inc., 2008. http://dx.doi.org/10.1002/9780470285251.

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Safe, Stephen, ed. Polychlorinated Biphenyls (PCBs): Mammalian and Environmental Toxicology. Berlin, Heidelberg: Springer Berlin Heidelberg, 1987. http://dx.doi.org/10.1007/978-3-642-70550-2.

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The ortho side of PCBs: Occurrence and disposition. Boston: Kluwer Academic, 1999.

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Japan-U.S. Joint Seminar on Toxicity of Chlorinated Biphenols, Dibenzofurans, Dibenzodioxins and Related Compounds (1983 Fukuoka, Japan). PCBS: Japan-U.S. symposium: April 25-28, 1983, Fukuoka, Japan. Research Triangle Park, N. Car: U.S. Dept. of Health and Human Services, 1985.

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Japan-U, S. Joint Seminar on Toxicity of Chlorinated Biphenols Dibenzofurans Dibenzodioxins and Related Compounds (1983 Fukuoka Japan). PCBS: Japan-U.S. symposium: April 25-28, 1983, Fukuoka, Japan. Research Triangle Park, N. Car: U.S. Dept. of Health and Human Services, 1985.

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Book chapters on the topic "Biochemical toxicology of PCBs"

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Jeffery, E. H. "Biochemical Mechanisms of Aluminum Toxicity." In Toxicology of Metals, 139–61. Berlin, Heidelberg: Springer Berlin Heidelberg, 1995. http://dx.doi.org/10.1007/978-3-642-79162-8_7.

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Smith, Susan Y., and Rana Samadfam. "Biochemical Markers of Bone Turnover." In Molecular and Integrative Toxicology, 175–201. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-56192-9_5.

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Bondy, S. C. "Biochemical Contributions to Neurotoxicology." In Recent Advances in Nervous System Toxicology, 43–65. Boston, MA: Springer US, 1988. http://dx.doi.org/10.1007/978-1-4613-0887-4_3.

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Isom, Gary E., and Joseph L. Borowitz. "Biochemical mechanisms of cyanide toxicity." In Toxicology of Cyanides and Cyanogens, 70–81. Chichester, UK: John Wiley & Sons, Ltd, 2016. http://dx.doi.org/10.1002/9781118628966.ch5.

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Borràs, Miquel, Santiago Llacuna, Assumpta Górriz, and Jacint Nadal. "Hematological and Biochemical Parameters in Pollution-Exposed Mice." In Archives of Toxicology, 189–95. Berlin, Heidelberg: Springer Berlin Heidelberg, 1998. http://dx.doi.org/10.1007/978-3-642-46856-8_17.

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Galli, Corrado L., and Marina Marinovich. "In Vitro Biochemical Markers of Skin Toxicity." In Skin Pharmacology and Toxicology, 165–79. Boston, MA: Springer US, 1990. http://dx.doi.org/10.1007/978-1-4684-7902-7_9.

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Zhang, Zhiyong, and Baohong Zhang. "Biochemical and Physiological Toxicity of Nanoparticles in Plant." In Environmental Toxicology and Toxicogenomics, 225–39. New York, NY: Springer US, 2021. http://dx.doi.org/10.1007/978-1-0716-1514-0_16.

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Hedili, A., J. M. Warnet, M. Thevenin, C. Martin, M. Yacoub, and J. R. Claude. "Biochemical Investigation of Atractylis Gummifera L. Hepatotoxicyty in the Rat." In Archives of Toxicology, 312–15. Berlin, Heidelberg: Springer Berlin Heidelberg, 1989. http://dx.doi.org/10.1007/978-3-642-74117-3_58.

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Wang, Dayong. "Endpoints for Assessing the Toxicity on Biochemical Processes." In Exposure Toxicology in Caenorhabditis elegans, 259–86. Singapore: Springer Singapore, 2020. http://dx.doi.org/10.1007/978-981-15-6129-0_9.

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Lugassy, Daniel, and Lewis Nelson. "Postmortem pathological and biochemical diagnosis of cyanide poisoning." In Toxicology of Cyanides and Cyanogens, 268–75. Chichester, UK: John Wiley & Sons, Ltd, 2016. http://dx.doi.org/10.1002/9781118628966.ch19.

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Conference papers on the topic "Biochemical toxicology of PCBs"

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Bodiguel, X., J. Tronczyński, V. Loizeau, C. Munschy, N. Guiot, A. M. Le Guellec, N. Olivier, F. Roupsard, and C. Mellon. "Classical and novel organohalogen compounds (PCBs and PBDEs) in hake (M. merluccius, L.) from the Mediterranean and Atlantic coasts (France)." In ENVIRONMENTAL TOXICOLOGY 2008. Southampton, UK: WIT Press, 2008. http://dx.doi.org/10.2495/etox080171.

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Sakhno, T. A., M. P. Semenenko, and V. N. Grin. "DYNAMICS OF BIOCHEMICAL INDICATORS OF BLOOD IN FRESH COWS ON THE BACKGROUND OF HEPATOPROTECTOR APPLICATION." In "International Scientific and Practical Conference" THEORY AND PRACTICE OF VETERINARY PHARMACY, ECOLOGY AND TOXICOLOGY IN AIC ", dedicated to the centenary of the Department of Pharmacology and Toxicology, SPbSUVM. FSBEI HE St. Petersburg SUVM, 2021. http://dx.doi.org/10.52419/3006-2021-2-211-212.

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Abstract:

The influence of a new injectable hepatoprotective drug livasen in the prevention of hepatosis in highly productive fresh cows has been studied. The performed pharmacoprophylaxis has shown high efficiency in the correction of diseases of the hepatobiliary system and metabolic insufficiency.

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Soulsby, Michael, Emily Johnson, Nisreen Akel, Rakhi Agarwal, Dana Gaddy, Maxim Dobretsov, Parimal Chowdhury, and Olga Tarasenko. "PANCREATIC HISTOLOGY AND ASSOCIATED BIOCHEMICAL CHANGES IN RATS ON HIND-LIMB SUSPENSION." In BIOLOGY, NANOTECHNOLOGY, TOXICOLOGY, AND APPLICATIONS: Proceedings of the 5th BioNanoTox and Applications International Research Conference. AIP, 2011. http://dx.doi.org/10.1063/1.3587463.

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