| Title: |
Toxic models of action of polychlorinated biphenyls in liver cells
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| Resource Type: |
document --> technical publication --> proceedings / conference paper(s)
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| Country: |
EU Projects
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| Year of publication: |
2003 |
| Availability: |
Machala, M. et al. (2003) Toxic models of action of polychlorinated biphenyls in liver cells. Persistent Toxic Substances Contamination of the European Region as a reflection of results of the GEF/UNEP Regional Based Assessment of Persistent Toxic Substances (RBA PTS) in Europe, the implementation of the Stockholm Convention and 'Community Strategy for Dioxins, Furans and PCBs
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| Author 1/Producer: |
Machala, M.
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| Other Authors/Producers: |
Plíšková, M., Bláha, L., Chramostová, K., Andrysík, Z., Pěnčíková, K., Vondráček, J.
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| Author / Producer Type: |
EC Project
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EUGRIS Keyword(s): |
Diffuse pollution-->Contaminants-->Persistent Organic Pollutants
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| Short description: |
PCBs have been reported to elicit multiple mechanisms of toxicity in various in vivo and in vitro systems. The following modes of action appear to be the most relevant to human and wildlife health: - disruption of endocrine functions including activation of aryl hydrocarbon and pregnane X receptors and consequent induction of xenobiotics-, steroid hormone- and fatty acid-metabolizing enzymes; modulations of sexual hormone signaling - effects on estrogen, androgen and progesterone receptors; disruption of thyroid hormone signaling; - tumor promotion (deregulation of cell proliferation and inhibition of GJIC); - neurotoxicity via modulation of ryanodine receptor and/or other neuronal signaling; - immunotoxicity (toxic effects on thymus mediated via AhR; arachidonic acid release leading to apoptosis of lymphocytes). Many of the adverse effects are mediated by activation of Ah receptor and toxic equivalency factors of PCB congeners are mostly based on the potency to activate this receptor. However, non-dioxin-like noncoplanar PCBs which are prevalent in the environment, elicit also several toxicologically relevant mechanisms which may lead to endocrine disruption, tumor promotion, neurotoxicity or immunotoxicity.
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Submitted By:
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Dr Stefan Gödeke WhoDoesWhat?
Last update: 14/02/2006
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