Protective effect of prostacyclin against pre-cardiac edema caused by 2,3,7,8-tetrachlorodibenzo- p -dioxin and a thromboxane receptor agonist in developing zebrafish

Nijoukubo, Daisuke; Tanaka, Yasuaki; Okuno, Yuki; Yin, Guojun; Kitazawa, Takio; Peterson, Richard E.; Kubota, Akira

doi:10.1016/j.chemosphere.2016.04.107

Cited by 10 publications

(8 citation statements)

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“…An initial step of dioxin-induced cardiovascular toxicity in zebrafish embryos occurring as early as 50 to 72 hr post fertilization (hpf) involves activation of aryl hydrocarbon receptor 2 (Ahr2), and the toxicity was explained, at least partially, by increasing vascular permeability (Dong et al, 2004) as well as structural and functional changes in the heart (Antkiewicz et al, 2005). Molecular mechanistic investigations further revealed the involvement of prostanoid signaling in dioxin-induced cardiovascular toxicity in zebrafish embryos (Teraoka et al, 2009(Teraoka et al, , 2014Nijoukubo et al, 2016). Some CYPs, including CYP1A, CYP1C1, CYP1C2 and CYP5A, have also been suggested to be involved in dioxin-induced cardiovascular toxicity in zebrafish embryos (Teraoka et al, 2003(Teraoka et al, , 2009Kubota et al, 2011).…”

Section: Introductionmentioning

confidence: 99%

Transcriptional profiling of cytochrome P450 genes in the liver of adult zebrafish, Danio rerio

et al. 2019

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Increasing use of zebrafish in biomedical, toxicological and developmental studies requires explicit knowledge of cytochrome P450 (CYP), given the central role of CYP in oxidative biotransformation of xenobiotics and many regulatory molecules. A full complement of CYP genes in zebrafish and their transcript expression during early development have already been examined. Here we established a comprehensive picture of CYP gene expression in the adult zebrafish liver using a RNAseq technique. Transcriptional profiling of a full complement of CYP genes revealed that CYP2AD2, CYP3A65, CYP1A, CYP2P9 and CYP2Y3 are major CYP genes expressed in the adult zebrafish liver in both sexes. Quantitative real-time RT-PCR analysis for selected CYP genes further supported our RNAseq data. There were significant sex differences in the transcript levels for CYP1A, CYP1B1, CYP1D1 and CYP2N13, with males having higher expression levels than those in females in all cases. A similar feature of gender-specific expression was observed for CYP2AD2 and CYP2P9, suggesting sex-specific regulation of constitutive expression of some CYP genes in the adult zebrafish liver. The present study revealed several "orphan" CYP genes as dominant isozymes at transcript levels in the adult zebrafish liver, implying crucial roles of these CYP genes in liver physiology and drug metabolism. The current results establish a foundation for studies with zebrafish in drug discovery and toxicology.

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Section: Introductionmentioning

confidence: 99%

Transcriptional profiling of cytochrome P450 genes in the liver of adult zebrafish, Danio rerio

et al. 2019

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“…The long-fin wild-type strain of zebrafish was used for all experiments, and the zebrafish were maintained as previously described (Nijoukubo et al, 2016). Adult zebrafish were obtained from a local pet shop.…”

Section: Zebrafishmentioning

confidence: 99%

“…Zebrafish larvae (5 dpf) were exposed to either dimethyl sulfoxide (DMSO) or different concentrations of dexamethasone dissolved in DMSO in 3 mL of Zebrafish Ringer solution (38.7 mM NaCl, 1.0 mM KCl, 1.7 mM HEPES-NaOH pH 7.2, 2.4 mM CaCl 2 ) in 3.5 cm diameter polystyrene Petri dishes (Nijoukubo et al, 2016). Twenty-four hours later, zebrafish were placed dorso-laterally in 3% carboxymethyl cellulose/Zebrafish Ringer solution, and images of 6 dpf larvae were taken under a microscope.…”

Section: Chemical Exposure and Observation Of Hepatomegalymentioning

confidence: 99%

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Dexamethasone-induced hepatomegaly and steatosis in larval zebrafish

Yin

Cao

et al. 2017

J. Toxicol. Sci.

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-Fish hepatobiliary syndrome, characterized by hepatomegaly and fatty liver, has been frequently reported in many cultured fish species and has caused a dramatic economic loss in China. Glucocorticoids are thought to be important non-nutritional factors for hepatomegaly and fatty liver development. In the present study, a dexamethasone-induced zebrafish model of fatty liver and hepatomegaly was established, and the role of glucocorticoid receptor (GR) in the development of hepatomegaly and fatty liver was investigated using developing zebrafish. Exposure of larval zebrafish at 5 days post fertilization (dpf) to dexamethasone for 24 hr caused significant increases of liver size and number of fish with hepatic steatosis at 6 dpf. The increase of liver size caused by dexamethasone was significantly reversed by treatment with RU486, a GR antagonist, and by gene knock-down with a morpholino against the GR. The dexamethasone-induced hepatic steatosis was also inhibited by treatment with RU486. Overall, the results highlight larval zebrafish as a useful model for stress-induced liver failure.

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“…TCDD-evoked early edema was almost blocked by both antioxidants and thromboxane receptor (TP) inhibitors [ 57 ]. We also showed that TP agonist-induced edema was antagonized by activation of the prostacyclin receptor (IP) but not by antioxidants [ 42 ]. These results suggest that both TP pathway and oxidative stress are involved in TCDD-induced circulation failure including edema, but the sites of their actions are different.…”

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confidence: 99%

Oxidative stress inducers potentiate 2,3,7,8-tetrachlorodibenzo-p-dioxin-mediated pre-cardiac edema in larval zebrafish

Tanaka

Adachi

Akasaka

et al. 2021

The Journal of Veterinary Medical Science

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We reported the involvement of oxidative stress and prostaglandins including thromboxane and prostacyclin in pre-cardiac edema (early edema) caused by 2,3,7,8-tetrachlorodibenzo- p -dioxin (TCDD). While the involvement of oxidative stress in TCDD-induced toxicity has been frequently reported, the mechanism of its action is still unclear. In the present study, oxidative stress inducers including paraquat, hydrogen peroxide (H 2 O 2 ) and rotenone augmented early edema (edema) induced by a low concentration of TCDD (0.1 ppb) at 55 hr post fertilization (hpf), while each of them alone did not cause edema. Edema caused by TCDD plus oxidative stress inducers was almost abolished by antioxidants, an antagonist for thromboxane receptor (ICI-192,605) and an agonist for prostacyclin receptor (beraprost), suggesting that the site of action of these inducers was in the regular signaling pathway after activation of aryl hydrocarbon receptor type 2 (AHR2) by TCDD. Oxidative stress inducers also enhanced edema caused by an agonist for the thromboxane receptor (U46619), and the enhancement was also inhibited by antioxidants. Sulforaphane and auranofin, activators of Nrf2 that is a master regulator of anti-oxidative response, did not affect U46619-evoked edema but almost abolished TCDD-induced edema and potentiation by paraquat in both TCDD- and U46619-induced edema. Taken together, the results suggest that oxidative stress augments pre-cardiac edema caused by TCDD via activation of thromboxane receptor-mediated signaling in developing zebrafish. As paraquat and other oxidative stress inducers used also are environmental pollutants, interaction between dioxin-like compounds and exogenous source of oxidative stress should also be considered.

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Protective effect of prostacyclin against pre-cardiac edema caused by 2,3,7,8-tetrachlorodibenzo- p -dioxin and a thromboxane receptor agonist in developing zebrafish

Cited by 10 publications

References 50 publications

Transcriptional profiling of cytochrome P450 genes in the liver of adult zebrafish, <i>Danio rerio</i>

Transcriptional profiling of cytochrome P450 genes in the liver of adult zebrafish, <i>Danio rerio</i>

Dexamethasone-induced hepatomegaly and steatosis in larval zebrafish

Oxidative stress inducers potentiate 2,3,7,8-tetrachlorodibenzo-<i>p</i>-dioxin-mediated pre-cardiac edema in larval zebrafish

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