Log in

Relevant bibliographies by topics / Biochemical toxicology of PCBs / Journal articles

To see the other types of publications on this topic, follow the link: Biochemical toxicology of PCBs.

Journal articles on the topic 'Biochemical toxicology of PCBs'

Author: Grafiati

Published: 4 June 2021

Last updated: 1 February 2022

Create a spot-on reference in APA, MLA, Chicago, Harvard, and other styles

Select a source type:

Consult the top 50 journal articles for your research on the topic 'Biochemical toxicology of PCBs.'

Next to every source in the list of references, there is an 'Add to bibliography' button. Press on it, and we will generate automatically the bibliographic reference to the chosen work in the citation style you need: APA, MLA, Harvard, Chicago, Vancouver, etc.

You can also download the full text of the academic publication as pdf and read online its abstract whenever available in the metadata.

Browse journal articles on a wide variety of disciplines and organise your bibliography correctly.

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.

Full text

APA, Harvard, Vancouver, ISO, and other styles

2

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.

Full text

Abstract:

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.

APA, Harvard, Vancouver, ISO, and other styles

3

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.

Full text

Abstract:

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.

APA, Harvard, Vancouver, ISO, and other styles

4

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.

Full text

Abstract:

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.

APA, Harvard, Vancouver, ISO, and other styles

5

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.

Full text

Abstract:

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.

APA, Harvard, Vancouver, ISO, and other styles

6

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.

Full text

APA, Harvard, Vancouver, ISO, and other styles

7

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.

Full text

APA, Harvard, Vancouver, ISO, and other styles

8

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.

Full text

APA, Harvard, Vancouver, ISO, and other styles

9

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.

Full text

APA, Harvard, Vancouver, ISO, and other styles

10

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.

Full text

APA, Harvard, Vancouver, ISO, and other styles

11

Buha, Aleksandra, and Vesna Matović. "Toxicology of Mixtures - Cd +PCBs Experimental Model." Toxicology and Forensic Medicine - Open Journal 1, no. 1 (November 29, 2016): e9-e11. http://dx.doi.org/10.17140/tfmoj-1-e004.

Full text

APA, Harvard, Vancouver, ISO, and other styles

12

Habermehl, G. "Polychlorinated Biphenyls (PCBs): Mammalian and environmental toxicology." Toxicon 27, no. 3 (January 1989): 399. http://dx.doi.org/10.1016/0041-0101(89)90192-x.

Full text

APA, Harvard, Vancouver, ISO, and other styles

13

Antunes-Fernandes, Elsa C., Toine F. H. Bovee, Frieda E. J. Daamen, Richard J. Helsdingen, Martin van den Berg, and Majorie B. M. van Duursen. "Some OH-PCBs are more potent inhibitors of aromatase activity and (anti-) glucocorticoids than non-dioxin like (NDL)-PCBs and MeSO2-PCBs." Toxicology Letters 206, no. 2 (October 2011): 158–65. http://dx.doi.org/10.1016/j.toxlet.2011.07.008.

Full text

APA, Harvard, Vancouver, ISO, and other styles

14

Selvakumar, Kandaswamy, Senthamilselvan Bavithra, Sekaran Suganya, Firdous Ahmad Bhat, Gunasekaran Krishnamoorthy, and Jagadeesan Arunakaran. "Effect of Quercetin on Haematobiochemical and Histological Changes in the Liver of Polychlorined Biphenyls-Induced Adult Male Wistar Rats." Journal of Biomarkers 2013 (October 1, 2013): 1–12. http://dx.doi.org/10.1155/2013/960125.

Full text

Abstract:

Polychlorinated biphenyls exposure damages the rat liver cells. Hematological parameters such as hemoglobin, packed cell volume, red-blood cells, white-blood cells, neutrophils, platelet counts, and RBC indices were significantly decreased. Polymorphs, eosinophil counts, and erythrocyte sedimentation rate were significantly increased. Serum liver enzymes such as aspartate transaminase, alanine transaminase, alkaline phosphatase, and gamma-glutamyl transferase were increased by PCBs treatment. Serum lipid profiles such as cholesterol, triglycerides, low-density lipoproteins and very-low-density lipoproteins were increased in PCBs-treated rats. High-density lipoprotein, total protein, albumin, globulin levels, and albumin/globulin ratio were also decreased after PCB exposure. Then levels of sodium, potassium, chloride, and bicarbonate were also altered. Serum glucose levels were increased along with total bilirubin after PCBs exposure. Simultaneous quercetin supplementation significantly protected the PCBs-induced changes of hematobiochemical parameters. Thus, quercetin shows a protective role against PCBs-induced alterations in the hematological and biochemical parameters.

APA, Harvard, Vancouver, ISO, and other styles

15

Krishnamoorthy, Gunasekaran, Kandaswamy Selvakumar, Prabhu Venkataraman, Perumal Elumalai, and Jagadeesan Arunakaran. "Lycopene supplementation prevents reactive oxygen species mediated apoptosis in Sertoli cells of adult albino rats exposed to polychlorinated biphenyls." Interdisciplinary Toxicology 6, no. 2 (June 1, 2013): 83–92. http://dx.doi.org/10.2478/intox-2013-0015.

Full text

Abstract:

Abstract Sertoli cell proliferation is attenuated before attaining puberty and the number is fixed in adult testes. Sertoli cells determine both testis size and daily sperm production by providing physical and metabolic support to spermatogenic cells. Polychlorinated biphenyls (PCBs) exposure disrupts functions of Sertoli cells causing infertility with decreased sperm count. On the other hand, lycopene is improving sperm count and motility by reducing oxidative stress in humans and animals. Hence we hypothesized that PCBs-induced infertility might be due to Sertoli cell apoptosis mediated by oxidative stress and lycopene might prevent PCBs-induced apoptosis by acting against oxidative stress. To test this hypothesis, animals were treated with vehicle control, lycopene, PCBs and PCBs + lycopene for 30 days. After the experimental period, the testes and cauda epididymidis were removed for isolation of Sertoli cells and sperm, respectively. We observed increased levels of oxidative stress markers (H2O2 and LPO) levels, increased expression of apoptotic molecules (caspase-8, Bad, Bid, Bax, cytochrome C and caspase-3), decreased anti-apoptotic (Bcl2) molecule and elevated apoptotic marker activity (caspase-3) in Sertoli cells of PCBs-exposed animals. These results were associated with decreased sperm count and motility in PCBs exposed animals. On the other hand, lycopene prevented the elevation of Sertoli cellular apoptotic parameters and prevented the reduction of sperm parameters (count and motility). The data confirmed that lycopene as an antioxidant scavenged reactive oxygen substances, prevented apoptosis, maintained normal function in Sertoli cells and helped to provide physical and metabolic support for sperm production, thereby treating infertility in men.

APA, Harvard, Vancouver, ISO, and other styles

16

Eum, Sung Yong, Ibolya E. András, Pierre-Olivier Couraud, Bernhard Hennig, and Michal Toborek. "PCBs and tight junction expression." Environmental Toxicology and Pharmacology 25, no. 2 (March 2008): 234–40. http://dx.doi.org/10.1016/j.etap.2007.10.019.

Full text

APA, Harvard, Vancouver, ISO, and other styles

17

Zhao, Zhe, and Lan Ying Zhang. "Screening and Identification of a PCBs-Degrading Halophilic Bacterium." Advanced Materials Research 113-116 (June 2010): 2177–80. http://dx.doi.org/10.4028/www.scientific.net/amr.113-116.2177.

Full text

Abstract:

Polychlorinated biphenyls (PCBs) are Persistent Organic Pollutants (POPs). This experiment screened a halophilic bacterium from the deep sea sediments, which could grow at the salinity of 15%, and designated as B2.6. The cells of this strain were rod shaped, Gram negative, motile. Growth of this bacterium in the presence of PCBs, as the sole source of carbon and energy, and the experiment indicated that at 30°C when pH value is between 7 and 8, inoculation amount is 5mL, the concentration of PCBs is below 3mg•L-1, and the ratio of degradation could reach 90% at 72h. The traditional morphology, physiological and biochemical properties as well as identified system of Biolog were applied to the bacterial classification. The pattern of PCBs-degrading enzyme production of strain B2.6 was continuous synthesis.

APA, Harvard, Vancouver, ISO, and other styles

18

Zhao, Zhe, Sheng Guang Zhuo, Xiu Yan Zhou, and Lan Ying Zhang. "Isolation and Identification of a PCBs-Degrading Strain." Advanced Materials Research 518-523 (May 2012): 229–32. http://dx.doi.org/10.4028/www.scientific.net/amr.518-523.229.

Full text

Abstract:

A salt-tolerant PCBs degrading strain B2.6 which can use PCBs as the sole carbon source and energy was isolated from the deep sea sediments of southern Yellow Sea. It was identified as Vibrio splendidus, according to morphological, physiological and biochemical characteristics and 16SrDNA sequence analysis. The experimental results suggested that the optimum conditions for the degradation of PCBs are temperature 30°C, pH 7 to 8, the concentration of NaCl was 150g•L-1. Under the optimum conditions, the PCBs degradation could reach 98.27% in 72h which concentration was below 0.6mg•L-1. The genome was amplified with bacterium 16SrDNA primer. The amplified product was purified and sequenced forphylogenetic analyses with Genbank. The bacterium B2.6 was identified as Vibrio splendidus. RAPD analyses of B2.6 produced stable DNA fingerprint. These studies have provided parameter for the further dynamic resolution of bacterium clusters for the rehabilitation of PCBs contaminated underground water environment with B2.6 PRB method.

APA, Harvard, Vancouver, ISO, and other styles

19

Furukawa, Kensuke. "Biochemical and genetic bases of microbial degradation of polychlorinated biphenyls(PCBs)." Journal of General and Applied Microbiology 46, no. 6 (2000): 283–96. http://dx.doi.org/10.2323/jgam.46.283.

Full text

APA, Harvard, Vancouver, ISO, and other styles

20

Safe, Stephen. "Polychlorinated biphenyls (PCBs): mutagenicity and carcinogenicity." Mutation Research/Reviews in Genetic Toxicology 220, no. 1 (January 1989): 31–47. http://dx.doi.org/10.1016/0165-1110(89)90007-9.

Full text

APA, Harvard, Vancouver, ISO, and other styles

21

Fischer, L. "Symposium Overview: Toxicity of Non-Coplanar PCBs, ,." Toxicological Sciences 41, no. 1 (January 1998): 49–61. http://dx.doi.org/10.1006/toxs.1997.2386.

Full text

APA, Harvard, Vancouver, ISO, and other styles

22

Uhler, Allen D., Jeffery H. Hardenstine, Deborah A. Edwards, and Guilherme R. Lotufo. "Leaching Rate of Polychlorinated Biphenyls (PCBs) from Marine Paint Chips." Archives of Environmental Contamination and Toxicology 81, no. 2 (July 1, 2021): 324–34. http://dx.doi.org/10.1007/s00244-021-00868-6.

Full text

Abstract:

AbstractPolychlorinated biphenyls (PCBs) were added to certain marine vessel bottom paints as a plasticizer to improve the adhesion and durability of the paint. The most common PCB formulation used to amend such paints was Aroclor 1254. Fugitive Aroclor-containing paint chips generated from vessel maintenance and repair operations represent a potential source of PCB contamination to sediments. Limited published studies indicate that Aroclor-containing paint is largely inert and exhibits low PCB leaching into water; however, the rate and degree of leaching of PCBs from paint chips have not been directly studied. This laboratory-based study evaluated the rate and extent of leaching of PCBs from paint chips into freshwater. The results of this investigation demonstrate that the rate of PCB dissolution from paint chips decreased rapidly and exponentially over time. Based on this study, it is estimated that the rate of leaching of PCBs from paint chips would cease after approximately 3 years of exposure to water. When all leachable PCBs were exhausted, it is estimated that less than 1% of the mass of PCBs in the paint chips was amenable to dissolution. The results of this experiment suggest that Aroclor-containing paint chips found in sediments are likely short-term sources of dissolved-phase PCB to pore or surface waters and that the majority of the PCBs in paint chips remain in the paint matrix and unavailable for partitioning into water. Graphic Abstract

APA, Harvard, Vancouver, ISO, and other styles

23

Brown, John F., Helen Feng, Donna L. Bedard, Michael J. Brennan, James C. Carnahan, and Ralph J. May. "Environmental dechlorination of PCBs." Environmental Toxicology and Chemistry 6, no. 8 (August 1987): 579–93. http://dx.doi.org/10.1002/etc.5620060802.

Full text

APA, Harvard, Vancouver, ISO, and other styles

24

BUCKMAN, A., C. WONG, E. CHOW, S. BROWN, K. SOLOMON, and A. FISK. "Biotransformation of polychlorinated biphenyls (PCBs) and bioformation of hydroxylated PCBs in fish." Aquatic Toxicology 78, no. 2 (June 15, 2006): 176–85. http://dx.doi.org/10.1016/j.aquatox.2006.02.033.

Full text

APA, Harvard, Vancouver, ISO, and other styles

25

Lim, Joe Jongpyo, Xueshu Li, Hans-Joachim Lehmler, Dongfang Wang, Haiwei Gu, and Julia Yue Cui. "Gut Microbiome Critically Impacts PCB-induced Changes in Metabolic Fingerprints and the Hepatic Transcriptome in Mice." Toxicological Sciences 177, no. 1 (June 16, 2020): 168–87. http://dx.doi.org/10.1093/toxsci/kfaa090.

Full text

Abstract:

Abstract Polychlorinated biphenyls (PCBs) are ubiquitously detected and have been linked to metabolic diseases. Gut microbiome is recognized as a critical regulator of disease susceptibility; however, little is known how PCBs and gut microbiome interact to modulate hepatic xenobiotic and intermediary metabolism. We hypothesized the gut microbiome regulates PCB-mediated changes in the metabolic fingerprints and hepatic transcriptome. Ninety-day-old female conventional and germ-free mice were orally exposed to the Fox River Mixture (synthetic PCB mixture, 6 or 30 mg/kg) or corn oil (vehicle control, 10 ml/kg), once daily for 3 consecutive days. RNA-seq was conducted in liver, and endogenous metabolites were measured in liver and serum by LC-MS. Prototypical target genes of aryl hydrocarbon receptor, pregnane X receptor, and constitutive androstane receptor were more readily upregulated by PCBs in conventional conditions, indicating PCBs, to the hepatic transcriptome, act partly through the gut microbiome. In a gut microbiome-dependent manner, xenobiotic, and steroid metabolism pathways were upregulated, whereas response to misfolded proteins-related pathways was downregulated by PCBs. At the high PCB dose, NADP, and arginine appear to interact with drug-metabolizing enzymes (ie, Cyp1–3 family), which are highly correlated with Ruminiclostridium and Roseburia, providing a novel explanation of gut-liver interaction from PCB-exposure. Utilizing the Library of Integrated Network-based Cellular Signatures L1000 database, therapeutics targeting anti-inflammatory and endoplasmic reticulum stress pathways are predicted to be remedies that can mitigate PCB toxicity. Our findings demonstrate that habitation of the gut microbiota drives PCB-mediated hepatic responses. Our study adds knowledge of physiological response differences from PCB exposure and considerations for further investigations for gut microbiome-dependent therapeutics.

APA, Harvard, Vancouver, ISO, and other styles

26

Šrédlová, Kamila, Kateřina Šírová, Tatiana Stella, and Tomáš Cajthaml. "Degradation Products of Polychlorinated Biphenyls and Their In Vitro Transformation by Ligninolytic Fungi." Toxics 9, no. 4 (April 8, 2021): 81. http://dx.doi.org/10.3390/toxics9040081.

Full text

Abstract:

Metabolites of polychlorinated biphenyls (PCBs)—hydroxylated PCBs (OH-PCBs), chlorobenzyl alcohols (CB-OHs), and chlorobenzaldehydes (CB-CHOs)—were incubated in vitro with the extracellular liquid of Pleurotus ostreatus, which contains mainly laccase and low manganese-dependent peroxidase (MnP) activity. The enzymes were able to decrease the amount of most of the tested OH-PCBs by > 80% within 1 h; the removal of more recalcitrant OH-PCBs was greatly enhanced by the addition of the laccase mediator syringaldehyde. Conversely, glutathione substantially hindered the reaction, suggesting that it acted as a laccase inhibitor. Hydroxylated dibenzofuran and chlorobenzoic acid were identified as transformation products of OH-PCBs. The extracellular enzymes also oxidized the CB-OHs to the corresponding CB-CHOs on the order of hours to days; however, the mediated and nonmediated setups exhibited only slight differences, and the participating enzymes could not be determined. When CB-CHOs were used as the substrates, only partial transformation was observed. In an additional experiment, the extracellular liquid of Irpex lacteus, which contains predominantly MnP, was able to efficiently transform CB-CHOs with the aid of glutathione; mono- and di-chloroacetophenones were detected as transformation products. These results demonstrate that extracellular enzymes of ligninolytic fungi can act on a wide range of PCB metabolites, emphasizing their potential for bioremediation.

APA, Harvard, Vancouver, ISO, and other styles

27

Battershill, Jon M. "Review of the Safety Assessment of Polychlorinated Biphenyls (PCBs) with Particular Reference to Reproductive Toxicity." Human & Experimental Toxicology 13, no. 9 (September 1994): 581–97. http://dx.doi.org/10.1177/096032719401300901.

Full text

Abstract:

1 The methods used to evaluate the toxicological effects of PCBs in animals have been reviewed. 2 The data show that Toxic Equivalency Factors (TEFs) could be developed to assess the potential toxicity of PCB mixtures for certain specific target organ effects (such as the liver and immune system) but would be inappropriate for other effects (e.g. thyroid function and neurochemical effects). More data on a wider range of individual PCB congeners and a method for systematically balancing toxicodynamic and toxicokinetic data are required before the TEF approach can be fully evaluated. 3 With the exception of the teratogenic effects seen in mice and the anti-oestrogenic effects reported in in vitro studies, there are insufficient data on individual PCB congeners to evaluate the structure-activity relationships for the effects of PCBs on reproduction. The data also show that individual PCBs may have opposing effects on a particular aspect of reproduction (for example individual PCB congeners may have either oestrogenic or anti-oestrogenic effects). Studies with individual PCB congeners have shown both enhancement and antagonism of the teratogenic effects of 2,3,7,8-tetrachloro dibenzo-p-dioxin (TCDD) in the mouse. It is not possible to use TEFs to evaluate the reproductive effects of PCBs. 4 The mechanism(s) responsible for the effects of PCBs on postnatal neurobehavioural development in rodents and monkeys have not been elucidated. At least two groups of PCBs which might be responsible for the observed effects have been identified in this review, one affecting the dopaminergic system and the other group affecting thyroid hormone levels. Considerably more research would be required before the TEF approach could be applied to the effects of PCBs on postnatal neurobehavioural development. This would include research on an appropriate animal model to determine whether the critical toxicological mechanism is mediated through the Ah receptor. 5 The reproductive toxicity of complex PCB mixtures such as those found in foods will depend on the identities and relative proportions of individual PCB congeners in the mixture. It is not possible to give an accurate estimate of a NOAEL or LOAEL from the reproduction studies using commercial PCB mixtures which could be readily applied to the safety assessment of PCBs present as contaminants in food. 6 It is concluded that the data presented in this paper support the hypothesis that there is no satisfactory method derived from the available studies in laboratory animals for evaluating the potential risk of adverse effects on reproduction posed by contamination of foods with PCBs.

APA, Harvard, Vancouver, ISO, and other styles

28

Kimbrough, Renate D. "Polychlorinated Biphenyls (PCBs) and Human Health: An Update." Critical Reviews in Toxicology 25, no. 2 (January 1995): 133–63. http://dx.doi.org/10.3109/10408449509021611.

Full text

APA, Harvard, Vancouver, ISO, and other styles

29

Kennedy, Conner L., Audrey Spiegelhoff, Kathy Wang, Thomas Lavery, Alexandra Nunez, Robbie Manuel, Lauren Hillers-Ziemer, Lisa M. Arendt, and Kimberly P. Keil Stietz. "The Bladder Is a Novel Target of Developmental Polychlorinated Biphenyl Exposure Linked to Increased Inflammatory Cells in the Bladder of Young Mice." Toxics 9, no. 9 (September 8, 2021): 214. http://dx.doi.org/10.3390/toxics9090214.

Full text

Abstract:

Bladder inflammation is associated with several lower urinary tract symptoms that greatly reduce quality of life, yet contributing factors are not completely understood. Environmental chemicals are plausible mediators of inflammatory reactions within the bladder. Here, we examine whether developmental exposure to polychlorinated biphenyls (PCBs) leads to changes in immune cells within the bladder of young mice. Female mice were exposed to an environmentally relevant mixture of PCBs through gestation and lactation, and bladders were collected from offspring at postnatal day (P) 28–31. We identify several dose- and sex-dependent PCB effects in the bladder. The lowest concentration of PCB (0.1 mg/kg/d) increased CD45+ hematolymphoid immune cells in both sexes. While PCBs had no effect on CD79b+ B cells or CD3+ T cells, PCBs (0.1 mg/kg/d) did increase F4/80+ macrophages particularly in female bladder. Collagen density was also examined to determine whether inflammatory events coincide with changes in the stromal extracellular matrix. PCBs (0.1 mg/kg/d) decreased collagen density in female bladder compared to control. PCBs also increased the number of cells undergoing cell division predominantly in male bladder. These results implicate perturbations to the immune system in relation to PCB effects on the bladder. Future study to define the underlying mechanisms could help understand how environmental factors can be risk factors for lower urinary tract symptoms.

APA, Harvard, Vancouver, ISO, and other styles

30

Nomiyama, Kei, Akifumi Eguchi, Kohki Takaguchi, Jean Yoo, Hazuki Mizukawa, Tomoko Oshihoi, Shinsuke Tanabe, and Hisato Iwata. "Targeted metabolome analysis of the dog brain exposed to PCBs suggests inhibition of oxidative phosphorylation by hydroxylated PCBs." Toxicology and Applied Pharmacology 377 (August 2019): 114620. http://dx.doi.org/10.1016/j.taap.2019.114620.

Full text

APA, Harvard, Vancouver, ISO, and other styles

31

Fawcett, HowardH. "PCBs the Environment." Journal of Hazardous Materials 31, no. 1 (June 1992): 89–90. http://dx.doi.org/10.1016/0304-3894(92)87042-e.

Full text

APA, Harvard, Vancouver, ISO, and other styles

32

Chen, Y. Q., S. De, S. Ghosh, and S. K. Dutta. "Congener-Specific Polychlorinated Biphenyl–Induced Cell Death in Human Kidney Cells In Vitro: Potential Role of Caspase." International Journal of Toxicology 25, no. 5 (September 2006): 341–47. http://dx.doi.org/10.1080/10915810600840859.

Full text

Abstract:

Polychlorinated biphenyls (PCBs) are among the most widespread and persistent pollutants in the global environment. Coplanar and noncoplanar PCBs have been shown to cause congener-specific apoptosis mediated neurotoxicity in rats. Very few, if any, such studies have been reported on human renal cell toxicity. The authors report here caspase-dependent or caspase-independent renal toxicity, as measured by apoptotic death induced by PCBs, depending on the planarity of congeners PCB-77 (coplanar) and PCB-153 (noncoplanar) in human kidney cells (HK2) in vitro. The authors have combined morphological and biological techniques to discover the relevance of apoptosis in renal proximal tubule cell death induced by these two PCB congeners. Treatment with both PCB congeners caused accelerated apoptosis in a time-and concentration-dependent manner. Based on our findings using human kidney (HK2) cells, there was more apoptosis-mediated loss of cell viability by non– ortho-substituted PCB-77 when compared to PCB-153. A significant increase of caspase-3 expression through immunoblot studies showed the involvement of apoptosis by PCB-77 compared to none by PCB-153. The broad-spectrum caspase inhibitor z-VAD-fmk showed increased cell death when treated by PCB-153, but not by PCB-77, confirming that caspase inhibitor induced a switch in the mode of cell death. It is reasonable to assume that apoptotic cell death in the renal proximal tubule cells treated by PCBs may have both caspase-dependent and caspase-independent pathways.

APA, Harvard, Vancouver, ISO, and other styles

33

Beier, Fabian, Andre Esser, Lucia Vankann, Anne Abels, Thomas Schettgen, Thomas Kraus, Tim H. Brümmendorf, and Patrick Ziegler. "Longitudinal changes in telomere length in PCB-exposed individuals: interaction with CMV infection." Archives of Toxicology 95, no. 4 (March 19, 2021): 1517–20. http://dx.doi.org/10.1007/s00204-021-03019-x.

Full text

Abstract:

AbstractWe recently demonstrated a significant shortening of age-adapted telomere length (TL) in lymphocytes of polychlorinated biphenyls (PCB)-exposed individuals. Here, we analyzed TL in individuals of the same PCB-exposed cohort during a 6-year follow-up period, investigating the change in TL between the first and second measurement as a function of time, concentration of PCBs and cytomegalovirus (CMV) infection. The age-adjusted TL of lymphocytes within the cohort of PCB-exposed individuals recovered from a first assessment in 2011 to a second assessment in 2017. Remarkably, if the concentration of lower chlorinated PCBs (LC PCBs) in 2011 was high (≥ 0.055 µg/L), the TL of CMV seropositive individuals remained significantly shortened both compared to age-adjusted controls as well as intra individually. This was confirmed by analysis of covariance as well as by multivariate linear mixed effects models. Since telomeres are responsive to various stress response pathways, including viral infection, we conclude that PCBs could contribute to immune senescence-like phenotypes associated with CMV infections and exacerbate negative aspects associated with the aging of the immune system.

APA, Harvard, Vancouver, ISO, and other styles

34

Selvakumar, Kandaswamy, Senthamilselvan Bavithra, Gunasekaran Krishnamoorthy, and Jagadeesan Arunakaran. "Impact of quercetin on tight junctional proteins and BDNF signaling molecules in hippocampus of PCBs-exposed rats." Interdisciplinary Toxicology 11, no. 4 (December 1, 2018): 294–305. http://dx.doi.org/10.2478/intox-2018-0029.

Full text

Abstract:

Abstract Polychlorinated biphenyls (PCBs) consist of a range of toxic substances which are directly proportional to carcinogenesis and tumor-promoting factors as well as having neurotoxic properties. Reactive oxygen species, which are produced from PCBs, alter blood–brain barrier (BBB) integrity, which is paralleled by cytoskeletal rearrangements and redistribution and disappearance of tight junction proteins (TJPs) like claudin-5 and occludin. Brain-derived neurotrophic factor (BDNF), plays an important role in the maintenance, survival of neurons and synaptic plasticity. It is predominant in the hippocampal areas vital to learning, memory and higher thinking. Quercetin, a flavonoid, had drawn attention to its neurodefensive property. The study is to assess the role of quercetin on serum PCB, estradiol and testosterone levels and mRNA expressions of estrogen receptor α and β, TJPs and BDNF signaling molecules on the hippocampus of PCBs-exposed rats. Rats were divided into 4 groups of 6 each. Group I rats were intraperitoneally (i.p.) administered corn oil (vehicle). Group II received quercetin 50 mg/kg/bwt (gavage). Group III received PCBs (Aroclor 1254) at 2 mg/kg bwt (i.p). Group IV received quercetin 50 mg/kg bwt (gavage) simultaneously with PCBs 2 mg/kg bwt (i.p.). The treatment was given daily for 30 days. The rats were euthanized 24 h after the experimental period. Blood was collected for quantification of serum PCBs estradiol and testosterone. The hippocampus was dissected and processed for PCR and Western blot; serum PCB was observed in PCB treated animals, simultaneously quercetin treated animals showed PCB metabolites. Serum testosterone and estradiol were decreased after PCB exposure. Quercetin supplementation brought back normal levels. mRNA expressions of estrogen α and β were decreased in the hippocampus of PCB treated rats. TJPS and BDNF signalling molecules were decreased in hippocampus of PCB treated rats. Quercetin supplementation retrieved all the parameters. Quercetin alone treated animals showed no alteration. Thus in PCB caused neurotoxicity, quercetin protects and prevents neuronal damage in the hippocampus.

APA, Harvard, Vancouver, ISO, and other styles

35

Corrigan, FM, M. French, and L. Murray. "Organochlorine compounds in human brain." Human & Experimental Toxicology 15, no. 3 (March 1996): 262–64. http://dx.doi.org/10.1177/096032719601500314.

Full text

Abstract:

Having observed polychlorinated biphenyls (PCBs) in brain tissue obtained post mortem from two men we have carried out a study of organochlorine compounds in frontal cortex from patients with Parkinson's disease (PD) and from controls. No PCBs were found in any of those samples. There was no difference in the concentra tion of the DDT metabolite pp'-DDE in the PD brain samples. Dieldrin (HEOD) was significantly decreased in PD brain when analysed by lipid weight. While these findings would not support the hypothesis that PCBs may contribute to the development of Parkinson's disease in humans it remains possible that they may cause damage to the basal ganglia before being displaced from brain tissue.

APA, Harvard, Vancouver, ISO, and other styles

36

Aluru, Neelakanteswar, Keegan S. Krick, Adriane M. McDonald, and Sibel I. Karchner. "Developmental Exposure to PCB153 (2,2’,4,4’,5,5’-Hexachlorobiphenyl) Alters Circadian Rhythms and the Expression of Clock and Metabolic Genes." Toxicological Sciences 173, no. 1 (October 17, 2019): 41–52. http://dx.doi.org/10.1093/toxsci/kfz217.

Full text

Abstract:

Abstract Polychlorinated biphenyls (PCBs) are highly persistent and ubiquitously distributed environmental pollutants. Based on their chemical structure, PCBs are classified into non-ortho-substituted and ortho-substituted congeners. Non-ortho-substituted PCBs are structurally similar to dioxin and their toxic effects and mode of action are well-established. In contrast, very little is known about the effects of ortho-substituted PCBs, particularly, during early development. The objective of this study is to investigate the effects of exposure to an environmentally prominent ortho-substituted PCB (2,2’,4,4’,5,5’-hexachlorobiphenyl; PCB153) on zebrafish embryos. We exposed zebrafish embryos to 3 different concentrations of PCB153 starting from 4 to 120 hours post-fertilization (hpf). We quantified gross morphological changes, behavioral phenotypes, gene expression changes, and circadian behavior in the larvae. There were no developmental defects during the exposure period, but starting at 7 dpf, we observed spinal deformity in the 10 μM PCB153 treated group. A total of 633, 2227, and 3378 differentially expressed genes were observed in 0.1 μM (0.036 μg/ml), 1 μM (0.36 μg/ml), and 10 μM (3.6 μg/ml) PCB153-treated embryos, respectively. Of these, 301 genes were common to all treatment groups. KEGG pathway analysis revealed enrichment of genes related to circadian rhythm, FoxO signaling, and insulin resistance pathways. Behavioral analysis revealed that PCB153 exposure significantly alters circadian behavior. Disruption of circadian rhythms has been associated with the development of metabolic and neurological diseases. Thus, understanding the mechanisms of action of environmental chemicals in disrupting metabolism and other physiological processes is essential.

APA, Harvard, Vancouver, ISO, and other styles

37

Burgin, Deborah E. "PCBs: Recent Advances in Environmental Toxicology and Health Effects." International Journal of Toxicology 21, no. 6 (November 2002): 511–12. http://dx.doi.org/10.1177/109158180202100610.

Full text

APA, Harvard, Vancouver, ISO, and other styles

38

Barron, M. G., H. Galbraith, and D. Beltman. "Comparative reproductive and developmental toxicology of PCBs in birds." Comparative Biochemistry and Physiology Part C: Pharmacology, Toxicology and Endocrinology 112, no. 1 (September 1995): 1–14. http://dx.doi.org/10.1016/0742-8413(95)00074-7.

Full text

APA, Harvard, Vancouver, ISO, and other styles

39

Hamilton, S. B. "Estrogenicity of environmental PCBs." Environmental Health Perspectives 103, no. 1 (January 1995): 12–13. http://dx.doi.org/10.1289/ehp.9510312a.

Full text

APA, Harvard, Vancouver, ISO, and other styles

40

Paasivirta, J., R. Herzschuh, T. Humppi, E. Kantolahti, J. Knuutinen, M. Lahtiperä, R. Laitinen, J. Salovaara, J. Tarhanen, and L. Virkki. "Pyrolysis products of PCBs." Environmental Health Perspectives 60 (May 1985): 269–78. http://dx.doi.org/10.1289/ehp.8560269.

Full text

APA, Harvard, Vancouver, ISO, and other styles

41

Vaidya, Vishal S., Kartik Shankar, Udayan M. Apte, Sharmilee P. Sawant, and Pallavi B. Limaye. "Introduction to Biochemical Toxicology." International Journal of Toxicology 20, no. 5 (September 2001): 331–33. http://dx.doi.org/10.1177/109158180102000511.

Full text

APA, Harvard, Vancouver, ISO, and other styles

42

Fry, Jeffrey R. "Book Review: Biochemical Toxicology." Alternatives to Laboratory Animals 14, no. 4 (June 1987): 397. http://dx.doi.org/10.1177/026119298701400418.

Full text

APA, Harvard, Vancouver, ISO, and other styles

43

Bridges, James W. "Frontiers in biochemical toxicology." Trends in Pharmacological Sciences 6 (January 1985): S11—S15. http://dx.doi.org/10.1016/0165-6147(85)90235-4.

Full text

APA, Harvard, Vancouver, ISO, and other styles

44

Tan, Y. "Ortho-Substituted PCBs Kill Cells by Altering Membrane Structure." Toxicological Sciences 80, no. 1 (March 10, 2004): 54–59. http://dx.doi.org/10.1093/toxsci/kfh119.

Full text

APA, Harvard, Vancouver, ISO, and other styles

45

Unyimadu, JP, O. Osibanjo, and JO Babayemi. "Polychlorinated biphenyls (PCBs) in River Niger, Nigeria: Occurrence, distribution and composition profiles." Toxicology and Industrial Health 34, no. 1 (November 22, 2017): 54–67. http://dx.doi.org/10.1177/0748233717736122.

Full text

Abstract:

Contamination of rivers with persistent organic pollutants (POPs) is an issue of current global concern. Polychlorinated biphenyls (PCBs) are POPs with origin from commercial, incineration and industrial sources. Hence, there is a need for monitoring their occurrence and distribution in the environment. This study assessed the occurrence, distribution and composition profiles of PCBs in River Niger, Nigeria. Surface and bottom water samples were collected in consecutive quarters for a period of 2 years, covering the beginning and end of the rainy seasons and the dry seasons, from five locations (Gurara, Lokoja, Onitsha, Brass and Nicolas) along River Niger. A total of 240 water samples were collected using a Van Dorn water sampler. EPA method 3510c was used with slight modifications for sample preparation and analysis. The PCBs were analysed using a Hewlett Packard GC 5890 Series 11 with electron capture detection, and confirmation was made using a Shimadzu GCMS QP2010. The higher molecular weight marker PCBs (∑CB 138, 153 and 180) were more dominant than the lighter homologues (∑CB 28, 52 and 101), while commercial sources Co-PCBs (80.8 ± 61.7 to 288.3 ± 102.0 ng L−1) were more dominant than the incineration sources (34.9 ± 3.82 to 75.5 ± 65.2 ng L−1). The POPs load in River Niger water varied in both time and space. In surface water of the River Niger, ∑PCBs were higher during the rainy season, as a result of storm run-off from land-based sources. In the Brass and Nicolas Rivers during the dry season, the ∑PCBs were higher during low tide. There was no noticeable pattern during the rainy season. It may be concluded from this study that the water of River Niger is not good for human consumption or abstraction of water from the river for drinking water treatment.

APA, Harvard, Vancouver, ISO, and other styles

46

Machala, Miroslav, Pavlina Simeckova, Lauy Al-Anati, Ulla Stenius, Katerina Pencikova, Jirina Prochazkova, Pavel Krcmar, Josef Slavik, and Jan Vondracek. "Effects of non-dioxin-like PCBs (NDL-PCBs) on signaling pathways contributing to liver tumor promotion and carcinogenesis." Toxicology Letters 189 (September 2009): S137. http://dx.doi.org/10.1016/j.toxlet.2009.06.726.

Full text

APA, Harvard, Vancouver, ISO, and other styles

47

Baars, A. J., M. I. Bakker, R. A. Baumann, P. E. Boon, J. I. Freijer, L. A. P. Hoogenboom, R. Hoogerbrugge, et al. "Dioxins, dioxin-like PCBs and non-dioxin-like PCBs in foodstuffs: occurrence and dietary intake in The Netherlands." Toxicology Letters 151, no. 1 (June 2004): 51–61. http://dx.doi.org/10.1016/j.toxlet.2004.01.028.

Full text

APA, Harvard, Vancouver, ISO, and other styles

48

Smith, Mary Alice. "Reassessment of the carcinogenicity of polychlorinated biphenyls (PCBS)." Journal of Toxicology and Environmental Health 50, no. 6 (April 1997): 567–79. http://dx.doi.org/10.1080/15287399709532055.

Full text

APA, Harvard, Vancouver, ISO, and other styles

49

Clare, Charlotte. "The state of play for PCBs." Food and Chemical Toxicology 27, no. 7 (January 1989): 493–94. http://dx.doi.org/10.1016/0278-6915(89)90039-2.

Full text

APA, Harvard, Vancouver, ISO, and other styles

50

Hunt, Gary, John Stegeman, and Larry Robertson. "PCBs: exposures, effects, remediation, and regulation with special emphasis on PCBs in schools." Environmental Science and Pollution Research 23, no. 3 (December 1, 2015): 1971–74. http://dx.doi.org/10.1007/s11356-015-5774-y.

Full text

APA, Harvard, Vancouver, ISO, and other styles

We offer discounts on all premium plans for authors whose works are included in thematic literature selections. Contact us to get a unique promo code!