2007
DOI: 10.1093/toxsci/kfm207
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Role of AHR2 in the Expression of Novel Cytochrome P450 1 Family Genes, Cell Cycle Genes, and Morphological Defects in Developing Zebra Fish Exposed to 3,3′,4,4′,5-Pentachlorobiphenyl or 2,3,7,8-Tetrachlorodibenzo-p-dioxin

Abstract: Halogenated agonists for the aryl hydrocarbon receptor (AHR), such as 3,3',4,4',5-pentachlorobiphenyl (PCB126) and 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), cause developmental toxicity in fish. AHR dependence of these effects is known for TCDD but only presumed for PCB126, and the AHR-regulated genes involved are known only in part. We defined the role of AHR in regulation of four cytochrome P450 1 (CYP1) genes and the effect of PCB126 on cell cycle genes (i.e., PCNA and cyclin E) in zebra fish (Danio rerio… Show more

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Cited by 138 publications
(184 citation statements)
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“…AHR activation during embryonic development leads to altered gene expression, malformations, and decreased survivorship (Billiard, Meyer, Wassenberg, Hodson, & Di Giulio, 2008; King‐Heiden et al., 2012). Experimental knockout or knockdown of AHR function protects against HAH‐ and PAH‐induced toxicity (Billiard, Timme‐Laragy, Wassenberg, Cockman, & Di Giulio, 2006; Clark, Matson, Jung, & Di Giulio, 2010; Fernandez‐Salguero, Hilbert, Rudikoff, Ward, & Gonzalez, 1996; Goodale et al., 2012; Incardona, Day, Collier, & Scholz, 2006; Incardona et al., 2005; Jönsson, Jenny, Woodin, Hahn, & Stegeman, 2007; Prasch et al., 2003); thus, evolved desensitization of this signaling pathway is plausibly causative for adaptive pollutant tolerance in killifish.…”
Section: Nature Of Parallel Pollution Adaptation In Killifishmentioning
confidence: 99%
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“…AHR activation during embryonic development leads to altered gene expression, malformations, and decreased survivorship (Billiard, Meyer, Wassenberg, Hodson, & Di Giulio, 2008; King‐Heiden et al., 2012). Experimental knockout or knockdown of AHR function protects against HAH‐ and PAH‐induced toxicity (Billiard, Timme‐Laragy, Wassenberg, Cockman, & Di Giulio, 2006; Clark, Matson, Jung, & Di Giulio, 2010; Fernandez‐Salguero, Hilbert, Rudikoff, Ward, & Gonzalez, 1996; Goodale et al., 2012; Incardona, Day, Collier, & Scholz, 2006; Incardona et al., 2005; Jönsson, Jenny, Woodin, Hahn, & Stegeman, 2007; Prasch et al., 2003); thus, evolved desensitization of this signaling pathway is plausibly causative for adaptive pollutant tolerance in killifish.…”
Section: Nature Of Parallel Pollution Adaptation In Killifishmentioning
confidence: 99%
“…Thus, AHR regulates adaptive and toxic responses to DLC and some PAH exposures in fish as in mammals, and loss of AHR function ameliorates these effects (Billiard et al., 2006; Goodale et al., 2012; Jönsson et al., 2007; Prasch et al., 2003). Despite the fundamental similarities, however, there are also differences in the AHR pathway among vertebrates—including fish—that may be important in their adaptive evolutionary response to pollution.…”
Section: Ahr Pathwaymentioning
confidence: 99%
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“…The latter was selected as a reference chemical as it represents one of the most abundant planar polychlorobiphenyl which can be found in the ng/L range in the environment (Ge et al, 2014). Moreover, its toxicity during zebrafish development is well described (Brown et al, 2002;Grimes et al, 2008;Jonsson et al, 2007a;Jonsson et al, 2012;Liu et al, 2015;. PCB126 is recognized as a strong inducer of biotransformation enzymes (i.e.…”
Section: Introductionmentioning
confidence: 99%
“…Expression of different genes known to be involved in PCB126 toxicity were studied in order to investigate whether the presence of PFASs would modify the patterns. Genes of the aryl hydrocarbon receptor (AhR) mediated pathway (ahr2, cyp1a) (Fang et al, 2012;Jonsson et al, 2007a;Jonsson et al, 2007b), the oxidative stress response (gpx1a) (Shi and Zhou, 2010), and a marker for apoptosis (tp53) (Shi et al, 2008) were studied. In order to address the possibility whether PFASs interfere with membrane integrity by altering lipid homeostasis, genes belonging to lipid metabolism (acaa2, osbpl1a) were monitored (Hu et al, 2005;Shi et al, 2009) Moreover, expression of two methyltransferases genes, dnmt1 and dnmt3ba, was measured in order to highlight underlying mechanisms of toxicity (Aluru et al, 2015 (Keiter et al, 2016): 25 mg/L (50µM) of PFOS, 15.7 mg/L (50 µM) of PFHxA and 7.5 µg/L (23 nM) of PCB126.…”
Section: Introductionmentioning
confidence: 99%