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pubmed-article:18378296pubmed:abstractTextPolycyclic aromatic hydrocarbons (PAHs) are contaminants increasing in the environment largely due to burning of fossil fuels. Our previous work identified a synergistic toxicity interaction in zebrafish embryos occurring when PAHs that are agonists for the aryl hydrocarbon receptor (AHR) co-occur with PAHs that are CYP1A inhibitors. This toxicity is mediated by the AHR2, and morpholino knockdown of CYP1A exacerbated toxicity. This study tested two hypotheses: (1) in the absence of functional CYP1A, metabolism of PAHs is shunted towards CYP1B1, which has been shown in mammals to produce more reactive metabolites of PAHs; alternatively, (2) CYP1B1 serves a protective role similar to CYP1A. We used a morpholino approach to knockdown CYP1B1 alone and in co-knockdown with CYP1A to determine whether we could alter deformities caused by synergistic toxicity of PAHs. CYP1B1 knockdown was not different from non-injected controls; nor were CYP1B1+CYP1A co-knockdown deformities different from CYP1A knockdown alone. These data suggest that CYP1B1 is not a significant factor in causing synergistic toxicity of PAHs, nor, in contrast to CYP1A, in providing protection.lld:pubmed
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pubmed-article:18378296pubmed:dateRevised2009-11-18lld:pubmed
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pubmed-article:18378296pubmed:articleTitleCYP1B1 knockdown does not alter synergistic developmental toxicity of polycyclic aromatic hydrocarbons in zebrafish (Danio rerio).lld:pubmed
pubmed-article:18378296pubmed:affiliationNicholas School of the Environment and Earth Sciences and Integrated Toxicology and Environmental Health Program, Duke University, Durham, NC, USA.lld:pubmed
pubmed-article:18378296pubmed:publicationTypeJournal Articlelld:pubmed
pubmed-article:18378296pubmed:publicationTypeResearch Support, U.S. Gov't, Non-P.H.S.lld:pubmed
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