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10. Cell-free, circulating microRNAs reflect air pollution-induced environmental health risks

Author

Krauskopf, J., van Veldhoven, K., Chadeau-Hyam, M., Vermeulen, R., Carrasco-Turigas, G., Nieuwenhuijsen, M., Vineis, P., de Kok, T. M., Kleinjans, J. C. S., Macro, International & Labour Economics, Toxicogenomics, RS: FSE MaCSBio, RS: FPN MaCSBio, RS: FHML MaCSBio, RS: MHeNs - R3 - Neuroscience, and RS: GROW - R1 - Prevention

Published
2019

12. Optimization of a 5-Fluorouracil-induced intestinal injury model in mice to construct a multi-scale predictive model of drug-induced intestinal toxicity

Author

Jardi, F., Van Heerden, M., Vereyken, L., Erkens, T., Rodrigues, D. F., Kleinjans, J. C. S., de Kok, T. M., Ferreria, S., Gardner, I., Fisher, C., Pritchard, M., Lynch, A., Sevin, D., Beattie, K., Pin, C., Lammens, L., de Jonghe, S., Toxicogenomics, RS: MHeNs - R3 - Neuroscience, RS: GROW - R1 - Prevention, RS: FSE MaCSBio, RS: FPN MaCSBio, and RS: FHML MaCSBio

Published
2019

16. Genes associated with Parkinson's disease respond to increasing polychlorinated biphenyl levels in the blood of healthy females

Author

Bohler, S., Espín-Pérez, A., Gebel, S., Bergdahl, Ingvar, Palli, D., Rantakokko, P., Kiviranta, H., Kyrtopoulos, S., Balling, R., Kleinjans, J. C. S., Bohler, S., Espín-Pérez, A., Gebel, S., Bergdahl, Ingvar, Palli, D., Rantakokko, P., Kiviranta, H., Kyrtopoulos, S., Balling, R., and Kleinjans, J. C. S.

Abstract

Supplement: 1Meeting Abstract: P12-03

Published
2018
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17. Circulating microRNAs as potential biomarkers of differential susceptibility to traumatic stress

Author

de Nijs, Laurence, Krauskopf, Julian, Snijders, C., Kleinjans, J. C S, Machiels, Barbie, Smeets, B., Kenis, G., Hove, Hanne D., Vinkers, C., Geuze, E., Boks, M., Vermetten, E., Rutten, B., de Nijs, Laurence, Krauskopf, Julian, Snijders, C., Kleinjans, J. C S, Machiels, Barbie, Smeets, B., Kenis, G., Hove, Hanne D., Vinkers, C., Geuze, E., Boks, M., Vermetten, E., and Rutten, B.

Published
2017

18. Circulating microRNAs as potential biomarkers of differential susceptibility to traumatic stress

Author

Huisartsopleiding Intern, Diagnostiek & Vroege Psychose Medisch, Brain, MGGZ, Onderzoeksgroep 2, de Nijs, Laurence, Krauskopf, Julian, Snijders, C., Kleinjans, J. C S, Machiels, Barbie, Smeets, B., Kenis, G., Hove, Hanne D., Vinkers, C., Geuze, E., Boks, M., Vermetten, E., Rutten, B., Huisartsopleiding Intern, Diagnostiek & Vroege Psychose Medisch, Brain, MGGZ, Onderzoeksgroep 2, de Nijs, Laurence, Krauskopf, Julian, Snijders, C., Kleinjans, J. C S, Machiels, Barbie, Smeets, B., Kenis, G., Hove, Hanne D., Vinkers, C., Geuze, E., Boks, M., Vermetten, E., and Rutten, B.

Published
2017

19. Cell line-specific oxidative stress in cellular toxicity: A toxicogenomics-based comparison between liver and colon cell models

Author

Deferme, L., Deferme, L., Briede, J. J., Claessen, S. M. H., Cavill, R., Kleinjans, J. C. S., Deferme, L., Deferme, L., Briede, J. J., Claessen, S. M. H., Cavill, R., and Kleinjans, J. C. S.

Abstract

Imbalance between high reactive oxygen species formation and antioxidant capacity in the colon and liver has been linked to increased cancer risk. However, knowledge about possible cell line-specific oxidative stress-mechanisms is limited. To explore this further, gene expression data from a human liver and colon cell line (HepG2/Caco-2), both exposed to menadione and H2O2 at six time points (0.5-1-2-4-8 and 24 h) were compared in association with cell cycle distribution. In total, 3164 unique- and 1827 common genes were identified between HepG2 and Caco-2 cells. Despite the higher number of unique genes, most oxidative stress-related genes such as CAT, OGG1, NRF2, NF-kappa B, GCLC, HMOX1 and GSR were differentially expressed in both cell lines. However, cell-specific regulation of genes such as KEAP1 and GCLM, or of the EMT pathway, which are of pathophysiological importance, indicates that oxidative stress induces different transcriptional effects and outcomes in the two selected cell lines. In addition, expression levels and/or -direction of common genes were often different in HepG2 and Caco-2 cells, and this led to very diverse downstream effects as confirmed by correlating pathways to cell cycle changes. Altogether, this work contributes to obtaining a better molecular understanding of cell line-specific toxicity upon exposure to oxidative stress-inducing compounds.

Published
2015

20. Abstracts of papers pharmacological meeting

Author

Boddeke, H. W. G. M., Jap, T. J. W., Hugtenburg, J. G., Veldsema-Currie, R. D., van Zwieten, P. A., Bom, A. H., Verdouw, P. P., Rutteman, A. M., Saxena, P. R., Davidesko, D., van Charldorp, K. J., Overhaus, P. H., Batink, H. D., Croiset, Gerda, Heijnen, Cobi J., de Wied, D., Drieman, J. C., Thijssen, H. H. W., Elands, J., Barberis, C., de Kloet, E. R., Engels, F., Henricks, P. A. J., v. d. Vliet, H., Nijkamp, F. P., Folkerts, Gert, Engels, Ferdi, Nijkamp, Frans P., Gouw, M. A. M., Wilffert, B., Heemskerk, F. M. J., Schrama, L. H., de Graan, P. N. E., Gispen, W. H., Hillege, J. L., van Gilst, W. H., Scholtens, E., van der Toren, W., Wesseling, H., Mathy, M -J., de Haan, N., Spanjer, W., Janssen, B, v Essen, H, Struyker-Boudier, H., Smits, J, Leurs, R., Go, J. N. L., Bast, A., Timmerman, H., Linthorst, A. C. E., Versteeg, D. H. G., Van den Buuse, M., De Jong, W., Post, M. J., te Biesebeek, J. D., Wemer, J., van Roolj, H. H., Prins, B., Koster, A. Sj., Sweep, C. G. J., Barna, I., Logtenberg, A. W., Wiegant, V. M., te Koppele, J. M., Coles, B., Ketterer, B., Mulder, G. J., Schoemaker, R., Debets, J., Smits, J., Smits, R. P. J. M., Steinbusch, H. W. M., Mulder, A. H., de Jonge, A., van Heiningen, P. N. M., Tierney, S. A. V, van Giersbergen, P. L. M., Tio, R. A., de Langen, C. D. J., de Graeff, P. A., van Luijtelaar, M. G. P. A., Tonnaer, J. D. A. M., van Oers, J. W. A. M., Tilders, F. J. H., van Hilten, J. A., Elliott, G. R., Bonta, I. L., van Hoogdalem, E. J., Geerts, J. A. M., de Boer, A. G., Breimer, D. D., Van Oosterhout, A. J. M., Van Rhee, A. M., Van Overveld, F. J., Houben, L. A. M. J., Terpstra, G. K., Raaijmakers, J. A. M., Bruijnzeel, P. L. B., van den Bos, R., Cools, A. R., Ögren, S -O., van den Dungen, H. M., van Rees, G. P., Schoemaker, J., van den Hooff, P., Seger, M. A., Burbach, J. P. H., Urban, I. J. A., v. d. Wouw, P. A., Vleeming, W., van Rooij, H. H., Porsius, A. J., Van der Zee, C. E. E. M., Edwards, P. M., De Koning, P., Verhaagen, J., Veenstro, D. M. J., Hozenberg, M. A. C. G., von Buuren, K. J. H., Vertagen, H., Thljssen, H. H. W., ten Hoor, F., Kleinjans, J. C. S., Verrijk, R., Vleemlng, W., Werner, J., Porslus, A. J., Voorhuis, Th. A. M., van Eekelen, J. A. M., Rosenfeld, P., Westphal, H. M., and Levine, S.

Published
1987
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21. Abstracts of papers toxicological meeting

Author

Beynen, A. C., Meijer, G. W., Joosten, H. F. P., van Kolfschoten, A. A., Koëter, H. B. W. M., Leegwater, P. C., Hermens, J. L. M., Rauws, A. G., Lumley, C. E., Walker, S. R., Bodar, C. W. M., Voogt, P. A., Wijnne, H., v. d. Zee, A., Zandee, D. I., Boogaard, P. J., Mulder, G. J., Nagelkerke, J. F., Boot, J. H., van Holsteijn, C. W. M., Blaauboer, B. J., Bos, R. P., Theuws, J. L. G., Jongeneelen, F. J., Brouwer, E. J., de Wolff, F. A., Busker, Ruud W., Commandeur, J. N. M., Vermeulen, N. P. E., Coosen, R., Schenk, E., van Leeuwen, F. X. R., Vos, J. G., Peereboom-Stegeman, J. H. J. Copius, van Veen, H., Pertijs, J., Danse, L. H. J. C., de Jong, K., Speijers, G. J. A., de Kom, J. F. M., Edelbroek, P. M., de Jong, E. G., Maes, R. A. A., de Vries, H., van Henegouwen, G. M. J. Beyersbergen, Berkhuysen, M. H. J., Kalloe, P., de Zwaan, A., de Kock, W. Chr, den Besten, P. J., Dogterom, P., Dormans, J. A. M. A., Boere, A. J. F., van Bree, L., Rombout, P. J. A., Evelo, C. T. A., Fijneman, P. H. S., Henderson, P. Th., Goeptar, A. R., Haenen, G. R. M. M., Bast, A., Tai Tin Tsoi, J. N. L., Timmerman, H., Hageman, G., Hermans, R., Kleinjans, J., Herweijer, M. A., Bootsman, T. C., van der Meer, S. G., Planta, R. J., Kappers, Frederike I., Wondergem-van Eijk, Jacqueline A. A. M., Kelder, P. P., de Mol, N. J., Janssen, L. H. M., Kroese, E. D., van de Poll, M. L. M, Meerman, J. H. N., Lock, R. A. C., Verbost, P. M., Flik, G., Bonga, S. E. Wendelaar, Lusthof, K. J., Hennes, W. C., den Hartogh, R., Kietjens, I., Dornans, J., Rombout, P., Schoonderwoerd, S. A., Luijendijk, J. J., van Henegouwen, G. M. J. Beijersbergen, te Koppele, J. M., Coles, B., Ketterer, B., van Ginkel, M. F., van der Voet, G. B., van Pelt, F. N. A. M., olde Meierink, Y. J. M., Weterings, P. J. J. H, van Os, C. H., Verhagen, H., Schutte, B., Reynders, M. M. J., Blijham, G. H., ten Hoor, F., Kleinjans, J. C. S., Wetzer, A. M., Weetink, H., Rietveld, E. C, Seutter-Berlage, F., and van Henegouwen, Gerard M. J. Beijersbergen

Published
1987
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22. Abstract of papers

Author

Konings, A. W. T., Joenje, H., Bast, A., Julicher, R., Van Iersel, A. A. J., Blaauboer, B. J., Balfoort, H. W., Ronbout, P. J. A., Borm, P. J. A., Engelen, J. J. M., Wouters, E. F. M., Swaen, C. M. H., de Boorder, Tj., Bos, R. P., Prinsen, W. J. C., Jongeneelen, F. J., Theuws, J. L. G., Henderson, P. Th., Cervantes, A., Schuurhuis, G. J., Pinedo, H. M., Lankelma, J., Commandeur, J. N. M., Oostendorp, R. A. J., Schoofs, P. R., Xu, B., Vermeulen, N. P. E., Coosen, R., van Leeuwen, F. X. R., Vos, J. G., Thijssen, J. H. H., Loeber, J. G., de Mol, N. J., Becht, A. B. C., Koenen, J., Lodder, G., de Wolff, F. A., van Ginkel, M. F., van der Voet, G. B., Dogterom, P., Nagelkerke, J. F., Mulder, G. J., Edelbroek, P. M., Zitman, F. G., Evelo, C. T. A., Niessen, H. J. J. M., Roelofs, H. M. J., Falke, H. E., De Groot, A. P., Willems, M. I., Franken, M. A. M., Kapteijn, R., Krajnc, E. I., Haenen, G. R. M. M., Plug, J. P. M., Timmerman, H., Hageman, G. J., Verhagen, H., Kleinjans, J. C. S., Herweijer, M. A., Bootsman, T. C., Scholte, B. J., Planta, R. J., Kroese, E. D., Tijdens, R. B., Meerman, J. H. N., Lusthof, K. J., Decuyper, J. G. A., Groothuis-Pielage, I. L., de Mol, N. J., Rietjens, I. M. C. M., Vos, R. M. E., Alink, G. M., van Bladeren, P. J., Rietveld, E. C., Ketels, H. H. T. M., Wetzer, A. M. A. C., Seutter-Berlage, F., Rombout, P., Dormans, J., van Bree, L., Marra, M., Til, H. P., Woutersen, R. A., Feron, V. J., Clary, J. J., Brandsma, A. E., de Wofff, F. A., van de Straat, R., de Vries, J., Boere, A. J. F., Rombout, P. J. A., Rietjens, I., Alink, G., van Erp, Yvette H. M., Heirbaut, Petra R. C. M., Koopmans, Marion J. E., Weterings, Peter J. J. M., van Loveren, H., de Klerk, A., Hakkert, B., Vertagen, H., Thijssen, H. H. W., Wester, P. W., Canton, J. H., Weterings, Peter J. J. M., and van Erp, Yvette H. M.

Published
1987
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23. Genomic analysis suggests higher susceptibility of children to air pollution

Author

Leeuwen, D. M., Marie Pedersen, Hendriksen, P. J. M., Boorsma, A., Herwijnen, M. H. M., Gottschalk, R. W. H., Kirsch-Volders, M., Lisbeth E. Knudsen, Sram, R. J., Bajak, E., Delft, J. H. M., Kleinjans, J. C. S., and TNO Kwaliteit van Leven

Subjects
Adult, Male, Parents, RNA Splicing, air pollution, data analysis, environmental exposure, environmental health, Physiological Sciences, cancer risk, immune response, Nuclear Family, blood analysis, gene expression profiling, genomics, micronucleus, Humans, controlled study, Genetic Predisposition to Disease, human, Child, Czech Republic, nucleosome, article, cancer susceptibility, parent, female, priority journal, Gene Expression Regulation, Health, child health, gene expression, RNA, Receptors, Chemokine, transcriptome
Abstract

Differences in biological responses to exposure to hazardous airborne substances between children and adults have been reported, suggesting children to be more susceptible. Aim of this study was to improve our understanding of differences in susceptibility in cancer risk associated with air pollution by comparing genome-wide gene expression profiles in peripheral blood of children and their parents. Gene expression analysis was performed in blood from children and parents living in two different regions in the Czech Republic with different levels of air pollution. Data were analyzed by two different approaches: one method first selected significantly differentially expressed genes and analyzed these gene lists for overrepresented biological processes, whereas the other applied the T-profiler tool to directly perform pathway analyses on the total gene set without preselection of significantly modulated gene expressions. In addition, gene expressions in both children and adults were investigated for associations with micronuclei frequencies. Both analysis approaches returned considerably more genes or gene groups and pathways that significantly differed between children from both regions than between parents. Very little overlap was observed between children and adults. The two most important biological processes or molecular functions significantly modulated in children, but not in adults, are nucleosome and immune response related. Our study suggests differences between children and adults in relation to air pollution exposure at the transcriptome level. The findings underline the necessity of implementing environmental health policy measures specifically for protecting children's health. © The Author 2008. Published by Oxford University Press. All rights reserved.

Published
2008

25. Genome-wide differential gene expression in children exposed to air pollution in the Czech Republic

Author

van Leeuwen, D M, van Herwijnen, M H M, Pedersen, Marie, Knudsen, Lisbeth E., Kirsch-Volders, M, Sram, R J, Staal, Y C M, Bajak, E, van Delft, J H M, Kleinjans, J C S, van Leeuwen, D M, van Herwijnen, M H M, Pedersen, Marie, Knudsen, Lisbeth E., Kirsch-Volders, M, Sram, R J, Staal, Y C M, Bajak, E, van Delft, J H M, and Kleinjans, J C S

Abstract

Udgivelsesdato: 2006-Aug-30, The Teplice area in the Czech Republic is a mining district where elevated levels of air pollution including airborne carcinogens, have been demonstrated, especially during winter time. This environmental exposure can impact human health; in particular children may be more vulnerable. To study the impact of air pollution in children at the transcriptional level, peripheral blood cells were subjected to whole genome response analysis, in order to identify significantly modulated biological pathways and processes as a result of exposure. Using genome-wide oligonucleotide microarrays, we investigated differential gene expression in children from the Teplice area (n=23) and compared them with children from the rural control area of Prachatice (n=24). In an additional approach, individual gene expressions were correlated with individual peripheral blood lymphocyte micronuclei frequencies, in order to evaluate the linkage of individual gene expressions with an established biomarker of effect that is representative for increased genotoxic risk. Children from the Teplice area showed a significantly higher average micronuclei frequency than Prachatice children (p=0.023). For considerable numbers of genes, the expression differed significantly between the children from the two areas. Amongst these genes, considerable numbers of genes were observed to correlate significantly with the frequencies of micronuclei. The main biological process that appeared significantly affected overall was nucleosome assembly. This suggests an effect of air pollution on the primary structural unit of the condensed DNA. In addition, several other pathways were modulated. Based on the results of this study, we suggest that transcriptomic analysis represents a promising biomarker for environmental carcinogenesis.

Published
2006

26. Benzo[a]pyrene-induced transcriptomic responses in primary hepatocytes and in vivo liver: Toxicokinetics is essential for in vivo–in vitro comparisons

Author

van Kesteren, P. C. E., primary, Zwart, P. E., additional, Schaap, M. M., additional, Pronk, T. E., additional, van Herwijnen, M. H. M., additional, Kleinjans, J. C. S., additional, Bokkers, B. G. H., additional, Godschalk, R. W. L., additional, Zeilmaker, M. J., additional, van Steeg, H., additional, and Luijten, M., additional

Published
2012
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40. Discrimination of genotoxic from non-genotoxic carcinogens by gene expression profiling

Author

van Delft, J. H. M., van Agen, E., van Breda, S. G. J., Herwijnen, M. H., Staal, Y. C. M., and Kleinjans, J. C. S.

Abstract

Two general mechanisms are implicated in chemical carcinogenesis. The first involves direct damage to DNA, referred to as genotoxic (GTX), to which the cell responds by repair of the damages, arrest of the cell cycle or induction of apoptosis. The second is non-DNA damaging, non-genotoxic (NGTX), in which a wide variety of cellular processes may be involved. Therefore, it can be hypothesized that modulation of the underlying gene expression patterns is profoundly distinct between GTX and NGTX carcinogens, and thus that expression profiling is applicable for classification of chemical carcinogens as GTX or NGTX. We investigated this hypothesis by analysing modulation of gene expression profiles induced by 20 chemical carcinogens in HepG2 cells with application of cDNA microarrays that contain 597 toxicologically relevant genes. In total, 22 treatments were included, divided in two sets. The training set consisted of 16 treatments (nine genotoxins and seven non-genotoxins) and the validation set of six treatments (three and three). Class discrimination models based on Pearson correlation analyses for the 20 most discriminating genes were developed with data from the training set, where after the models were tested with all data. Using all data, the correctness for classification of the carcinogens from the training set was clearly better than that for the validation set, namely 81 and 33%, respectively. Exclusion of the treatments that had only marginal effects on the expression profiles, improved the discrimination for the training and validation sets to 92 and 100% correctness, respectively. Exclusion of the gene expression signals that were hardly altered also improved classification, namely to 94 and 80%. Therefore, our study proves the principle that gene expression profiling can discriminate carcinogens with major differences in their mode of actions, namely genotoxins versus non-genotoxins.

Published
2004
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41. A molecular dosimetry approach to assess human exposure to environmental tobacco smoke in pubs.

Author

Besaratinia, A, Maas, L M, Brouwer, E M C, Moonen, E J C, De Kok, T M C M, Wesseling, G J, Loft, S, Kleinjans, J C S, and Van Schooten, F J

Abstract

Although the involvement of environmental tobacco smoke (ETS) in human lung cancer is no longer a matter of dispute, the magnitude of its impact still is. This is mainly due to the inefficiency of methodology to assess exposure to ETS especially in public places. Setting a real life exposure condition (3 h stay in local pubs) and using a matched-control study design, we quantified smoke-related DNA adducts in induced sputum and peripheral blood lymphocytes (PBL) of healthy non-smokers (n = 15) before and after a single pub visit by means of the (32)P-post-labeling assay. For verification, we also measured a spectrum of polycyclic aromatic hydrocarbons (PAH) in the ambient air of the pubs by personal air monitors, and determined the plasma concentrations of nicotine and cotinine by gas chromatography/mass spectrometry. The ambient air concentrations of all PAH were several orders of magnitude higher than those already reported for other indoor environments. The plasma concentrations of both nicotine and cotinine increased significantly after the pub visit (P = 0.001 and P = 0.0007, respectively). Accordingly, the overall DNA adduct profile in induced sputum, but not in PBL, changed quantitatively and qualitatively after the pub visit. Of most significance was the formation of a distinct DNA adduct in induced sputum of three individuals consequent to ETS exposure. This adduct co-migrated with the standard (+/-)-anti-benzo[a]pyrene diol epoxide-DNA adduct, which is known to form at lung cancer mutational hotspots. We conclude that real life exposure to ETS can give rise to pro-mutagenic lesions in the lower airway, and this can be best investigated in a relevant surrogate matrix such as induced sputum.

Published
2002
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42. Putative susceptibility markers of coronary artery disease: association between VDRgenotype, smoking, and aromatic DNA adduct levels in human right atrial tissue

Author

Schouten, F. J., Hirvonen, A., Maas, L. M., Mol, B. A., Kleinjans, J. C. S., Bell, D. A., and Durrer, J. D.

Abstract

Cancer and cardiovascular diseases share risk factors such as smoking, and the onset of both diseases have been suggested to have a common mechanistic basis. The binding of carcinogens to DNA (carcinogen‐DNA adducts), genetic polymorphisms in carcinogen‐detoxifying enzymes glutathione S‐transferases (GSTs), and genetic polymorphisms in the vitamin D receptor (VDR) are among the candidates for modifiers of cancer risk. We determined whether these biomarkers could be related to individual characteristics of patients suffering from cardiovascular diseases. For that purpose, DNA from the right atrial appendage of 41 patients who underwent open heart surgery was analyzed for smoking‐related DNA adducts and polymorphisms in GSTM1, GSTT1, and VDRgenes. Statistical analysis was used to identify any patient's characteristics associated with these molecular markers. Our results showed that heart tissue of cigarette smokers contained a variety of aromatic DNA adducts in significantly elevated levels compared to ex‐smokers (P<0.01) or nonsmokers (P<0.001). A linear relationship was observed between DNA adduct levels and daily cigarette smoking (rs=0.73; P=0.0003). Since cardiac myocytes are terminally differentiated cells that have lost their ability to divide and seemingly have limited DNA repair capacities, their levels might accumulate with time and thereby affect heart cell function or viability. Substantial interindividual differences between DNA adduct levels were observed, and persons with severe coronary artery disease (CAD), as assessed by coronary angiography, had higher DNA adduct levels than persons with no or mild CAD (P=0.04). As polymorphisms in GSTgenes have been shown to modulate DNA adduct levels and risk for lung cancer in smokers, we explored for the first time whether the GSTpolymorphisms could also explain deviating heart DNA adduct levels and CAD risk. However, no relation could be found between these covariants. In contrast, a VDRgenotype, which has been associated with decreased serum levels of the active hormonal form of vitamin D and increased risk for certain cancers, seemed to be related to severity of CAD (P=0.025). Our findings support the hypothesis that smoking‐related DNA damage may be involved in the onset of cardiovascular diseases and suggest that VDRgenotype may be a useful susceptibility marker of CAD.—van Schooten, F. J., Hirvonen, A., Maas, L. M., de Mol, B. A., Kleinjans, J. C. S., Bell, D. A., Durrer, J. D. Putative susceptibility markers of coronary artery disease: association between VDRgenotype, smoking, and aromatic DNA adduct levels in human right atrial tissue. FASEB J.12, 1409–1417 (1998)

Published
1998
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43. Blood Pressure Response to Chronic Low-Dose Intrarenal Noradrenaline Infusion in Conscious Rats

Author

Kleinjans, J. C. S., Smits, J. F. M., Kasbergen, C. M., Vervoort-Peters, H. T. M., and Boudier, H. A. J. Struyker

Abstract

1. Sodium chloride solution (0.9%) or noradrenaline in doses of 4, 12 and 36 μgh−1 kg−1 was infused for five consecutive days, either intrarenally (by a new technique) or intravenously into rats with one kidney removed. 2. Intrarenal infusion of noradrenaline caused hypertension at doses which did not do so when infused intravenously. 3. Intrarenal compared with intravenous infusion of noradrenaline caused higher plasma noradrenaline concentrations and a shift of the plasma noradrenaline concentration-blood pressure effect curve towards lower plasma noradrenaline levels. 4. These results suggest that hypertension after chronic intrarenal noradrenaline infusion is produced by relatively higher levels of circulating noradrenaline and by triggering of an additional intrarenal pressor mechanism.

Published
1983
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48. Determination of polycyclic aromatic hydrocarbons (PAH) and their metabolites in blood, feces, and urine of rats orally exposed to PAH contaminated soils

Author

Kleinjans, J. C. S., van Schooten, F. J., van der Wal, L., Moonen, E. J. C., and Levels, P.

Subjects
BIOLOGICAL monitoring, METABOLISM, POLYCYCLIC aromatic hydrocarbons, RATS, SOIL pollution
Abstract

Polycyclic aromatic hydrocarbons (PAH) have become an ubiquitous upper soil component as a consequence of industrialization involving a multitude of combustion processes. Ingestion of PAH contaminated soil is considered to be a major exposure route, specifically for small children living on these soils. Health risk assessment is based on extrapolations from data obtained via studies performed with pure chemicals. Additionally it is assumed that after oral intake all PAH presentin the soil will be absorbed by the human body. Interactions with the soil matrix, however, may modulate the bioavailability of PAH. In this study, we examined the absorption and excretion of PAH in rats orally exposed either to industrially contaminated soils or pure model compounds as anthracene, pyrene and benzo(a)pyrene (B[a]P). The modelcompounds and the metabolites, 1-hydroxypyrene (1-OH-pyrene) and 3-hydroxybenzo(a)pyrene (3-OH-B[a]P), were measured in blood, feces or urine by means of HPLC with fluorescence detection. Because of rapid biotransformation only minimal levels of unmetabolized anthracene, pyrene and B[a]P in blood could be detected. The pharmacokinetic parameters were nonlinear and suggestive of enterohepatic cycling. Only low levels of the compounds were excreted unchanged in feces whereas the levels of the metabolites were considerably higher in feces and urine. These results indicate that the dosed PAH are largely absorbed by the gastrointestinal tract, subsequently metabolized and excreted as metabolites via urine and feces. Significant differences between the soil-treated group and the pure mixture-treated group could be observed; the soil-treated group showed higher fecal excretion of unchanged pyrene (0.5 versus 0.2% of the original dose) and B[a]P (1 versus 0.3%), lower excretion of 1-OH-pyrene in feces (5.1 versus 17.0%), and lower excretion of 1-OH-pyrene in urine (0.2 versus 3.4%). The fecal excretion of 3-OH-B[a]P between the two groups was similar (8.8 versus8. [ABSTRACT FROM AUTHOR]

Published
1997

50. Circulating microRNAs as potential biomarkers for psychiatric and neurodegenerative disorders.

Author

van den Berg MMJ, Krauskopf J, Ramaekers JG, Kleinjans JCS, Prickaerts J, and Briedé JJ

Subjects
Alzheimer Disease blood, Alzheimer Disease diagnosis, Central Nervous System Diseases blood, Central Nervous System Diseases diagnosis, Humans, Neurodegenerative Diseases diagnosis, Biomarkers blood, Circulating MicroRNA blood, MicroRNAs blood, Neurodegenerative Diseases blood
Abstract

Circulating microRNAs (cimiRNAs) are a class of non-encoding RNAs found in bodily fluids such as blood, cerebrospinal fluid (CSF) and tears. CimiRNAs have been implicated as promising biomarkers for central nervous system (CNS) disorders because they are actively secreted as messengers and are profoundly involved in fine-tuning of developmental and differentiation processes. Furthermore, they are attractive biomarkers because they are extremely stable, tissue enriched and can be determined in a quantitative manner. This review aims to provide a comprehensive assessment on the current progress regarding the potential value of cimiRNAs as CNS biomarkers. Within this framework five CNS disorders are explored which share a common pathological hallmark namely cognitive impairment. The CNS disorders include Major depression disorder (MDD), Bipolar disorder (BD), Schizophrenia (SZ), Alzheimer's disease (AD) and Parkinson disease (PD). The similarities and differences between altered cimiRNAs in the different disorders are described. The miR-29 family, miR-34a-5p and miR-132-3p are discussed as common dysregulated cimiRNAs found in the CNS disorders. Furthermore, it is shown that the type of bodily fluid used for measuring cimiRNAs is important as inconsistencies in cimiRNAs expression directions are found when comparing CSF, blood cell-free and blood cell-bound samples., (Copyright © 2019 Elsevier Ltd. All rights reserved.)

Published
2020
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