Developmental toxicity of hydroxylated chrysene metabolites in zebrafish embryos

Diamante, Graciel; Müller, Gabrielle do Amaral e Silva; Menjivar-Cervantes, Norma; Xu, Elvis Genbo; Volz, David C.; Bainy, Afonso Celso Dias; Schlenk, Daniel

doi:10.1016/j.aquatox.2017.05.013

Cited by 47 publications

(31 citation statements)

References 40 publications

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“…Using the above‐mentioned modifications, Blackburn and co‐workers were able to assess correctly the mutagenicity potency of 18 PS samples from different product categories (Blackburn et al, ). Furthermore, hamster liver microsomes, and not hamster S9 fractions, were used in the present study because the activity of cytochrome P450 enzymes in hamster liver microsomes (expressed in nmol/mg protein) is three times higher than in the hamster S9 fractions (Appendix E; see Supporting Information), while it was assumed that particularly cytochrome P450‐mediated biotransformation to hydroxylated metabolites would bioactivate the PAHs (Diamante et al, ; Geier et al, ). The results obtained for 3OH‐BaP support this assumption, while DBA did not need bioactivation.…”

Section: Discussionmentioning

confidence: 99%

The role of metabolism in the developmental toxicity of polycyclic aromatic hydrocarbon‐containing extracts of petroleum substances

Kamelia

Haan

Spenkelink

et al. 2019

J of Applied Toxicology

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In vitro assays presently used for prenatal developmental toxicity (PDT) testing only assess the embryotoxic potential of parent substances and not that of potentially embryotoxic metabolites. Here we combined a biotransformation system, using hamster liver microsomes, with the ES‐D3 cell differentiation assay of the embryonic stem cell test (EST) to compare the in vitro PDT potency of two 5‐ring polycyclic aromatic hydrocarbons (PAHs), benzo[a]pyrene (BaP) and dibenz[a,h]anthracene (DBA), and dimethyl sulfoxide extracts from five PAH‐containing petroleum substances (PS) and a gas‐to‐liquid base oil (GTLb), with and without bioactivation. In the absence of bioactivation, DBA, but not BaP, inhibited the differentiation of ES‐D3 cells into beating cardiomyocytes in a concentration‐dependent manner. Upon bioactivation, BaP induced in vitro PDT, while its major metabolite 3‐hydroxybenzo[a]pyrene was shown to be active in the EST as well. This means BaP needs biotransformation to exert its embryotoxic effects. GTLb extracts tested negative in the EST, with and without bioactivation. The PS‐induced PDT in the EST was not substantially changed following bioactivation, implying that metabolism may not play a crucial role for the PS extracts under study to exert the in vitro PDT effects. Altogether, these results indicate that although some PAH require bioactivation to induce PDT, some do not and this latter appears to hold for the (majority of) the PS constituents responsible for the in vitro PDT of these complex substances.

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Section: Discussionmentioning

confidence: 99%

The role of metabolism in the developmental toxicity of polycyclic aromatic hydrocarbon‐containing extracts of petroleum substances

Kamelia

Haan

Spenkelink

et al. 2019

J of Applied Toxicology

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“…Zebrafish is deemed as a great vertebrate model for toxicity assessment [19][20][21][22][23][24]. The cardiovascular, nervous, and visual systems of zebrafish are similar to that of mammalian at the physiological and molecular levels [25][26][27][28].…”

Section: J O U R N a L P R E -P R O O Fmentioning

confidence: 99%

α-asarone induces cardiac defects and QT prolongation through mitochondrial apoptosis pathway in zebrafish

Shang

Dang

et al. 2020

Toxicology Letters

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“…13 Additionally, chrysene is capable of triggering the perturbation of DNA repair machinery. 16 Moreover, hydroxylated chrysene metabolites are reported to show developmental toxicity in Zebrafish Embryos, 17 and the connection between chrysene and cancer has also been revealed by several previous studies. 18 Nevertheless, there is little evidence to illustrate the association between chrysene and COPD.…”

Section: Introductionmentioning

confidence: 86%

Chrysene accelerates the proceeding of chronic obstructive pulmonary disease with the aggravation of inflammation and apoptosis in cigarette smoke exposed mice

Gao

Zhou

et al. 2020

Hum Exp Toxicol

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Chrysene, one of the basic polycyclic aromatic hydrocarbons (PAHs), has been reported to make damages to human health and living environment. Chronic obstructive pulmonary disease (COPD) is a progressive disorder with high morbidity and mortality. To investigate the role of chrysene in the development of COPD, male C57BL/6 mice were exposed to the cigarette smoke (CS) followed with the administration of chrysene. Morphological analyses indicated that chrysene caused earlier and severer pathological changes in CS-exposed mice. Besides, CS-exposed mice with chrysene treatment showed obvious collagen deposition, elevated α-smooth muscle actin (α-SMA) expression and reduced E-cadherin abundance at earlier stage, which suggested the acceleration and aggravation of pulmonary fibrosis. Moreover, quantification of leukocytes and pro-inflammatory cytokines in bronchoalveolar lavage fluid (BALF) and lung tissues implied that chrysene significantly exacerbated the proceeding of inflammation in CS-exposed mice. Furthermore, significantly increased apoptotic rates, augmented expressions of apoptotic related proteins and highly expressed TRPV1 were determined in CS-exposed mice with chrysene treatment, which indicated the association between COPD pathogenesis and TRPV1 channel. In summary, our findings elucidate that chrysene accelerates the development of COPD in a murine model with new molecular mechanisms.

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Developmental toxicity of hydroxylated chrysene metabolites in zebrafish embryos

Cited by 47 publications

References 40 publications

The role of metabolism in the developmental toxicity of polycyclic aromatic hydrocarbon‐containing extracts of petroleum substances

The role of metabolism in the developmental toxicity of polycyclic aromatic hydrocarbon‐containing extracts of petroleum substances

α-asarone induces cardiac defects and QT prolongation through mitochondrial apoptosis pathway in zebrafish

Chrysene accelerates the proceeding of chronic obstructive pulmonary disease with the aggravation of inflammation and apoptosis in cigarette smoke exposed mice

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