Basal and induced EROD activity in the chorioallantoic membrane during chicken embryo development

Self Cite

Polycyclic aromatic hydrocarbons (PAHs) are widespread in the environment and birds may be exposed to PAHs via diet, from preening feathers contaminated with oil, or through contamination of the eggshell during embryo development. In the present study, tissue distribution and the cell-specific binding of two labeled PAHs, benzo[a]pyrene ([3H]BaP) and 7,12-dimethylbenz[a]anthracene ([3H]DMBA), were examined in chicken embryos exposed in ovo to CYP1A inducers. Tape-section autoradiograms revealed high concentrations of radioactivity in the bile, liver, kidneys, heart, and leptomeninges. Light microscopy autoradiography of solvent-extracted tissue slices showed a high and selective binding in endothelial cells in certain blood vessels in brain, heart, lung, and chest muscle. Binding was also observed in blood vessel endothelial cells in the chorioallantoic membrane (CAM), an extraembryonal tissue lining the eggshell. Endothelial binding was confirmed in CAM exposed in vitro, implying that tissue-binding metabolites were formed in situ. The CYP1A inhibitor ellipticine abolished bleeding in the target endothelial cells in CAM. It is thus concluded that blood vessel endothelia in various tissues in birds can bioactivate environmental contaminants and be targets for their toxicity. In view of its critical position beneath the shell, the CAM could be an important target for toxicants following external exposure in oviparous species.

Section: Discussionmentioning

confidence: 82%

Section: Light-microscopy Autoradiography In Vivomentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Formation of benzo[a]pyrene and 7,12‐dimethylbenz[a]anthracene adducts in vascular endothelia of cytochrome P4501A–induced chicken embryos

Granberg¹,

Brunström²,

Brandt³

2003

Self Cite

“…Both the yolk sac and chorioallantoic membrane (the latter analogous to the placenta in mammals) are known to have CYP-enzyme activity and can act as a first defense against contaminant exposure (Annas et al 1999 and references therein). The chorioallantoic membrane only forms 4 to 5 d after incubation commences, suggesting that either its precursor mesodermal layers (Annas et al 1999) or the yolk sac membrane may have contributed to TPHP metabolism in the early quail eggs (as well as thereafter). Su et al (2016) showed that base catalyzed hydrolysis occurs to a minor degree in aqueous solutions at pH of 8 to 9, which is in the range of the present quail eggs (pH 7.9-9.2 [Romanoff and Romanoff 1929]).…”

Section: Mechanisms Of Tphp Metabolism In the Embryonated Quail Eggmentioning

confidence: 99%

“…The second possibility is that nonembryonic elements of the egg may have been responsible for enzymatic breakdown of TPHP in the first 2 d following injection. Both the yolk sac and chorioallantoic membrane (the latter analogous to the placenta in mammals) are known to have CYP-enzyme activity and can act as a first defense against contaminant exposure (Annas et al 1999 and references therein). The chorioallantoic membrane only forms 4 to 5 d after incubation commences, suggesting that either its precursor mesodermal layers (Annas et al 1999) or the yolk sac membrane may have contributed to TPHP metabolism in the early quail eggs (as well as thereafter).…”

Section: Mechanisms Of Tphp Metabolism In the Embryonated Quail Eggmentioning

confidence: 99%

Uptake, Deposition, and Metabolism of Triphenyl Phosphate in Embryonated Eggs and Chicks of Japanese Quail (Coturnix japonica)

Marteinson

Guigueno

Fernie

et al. 2020

The toxicokinetics of triphenyl phosphate (TPHP) in vivo including the uptake, deposition, and biotransformation into the metabolite diphenyl phosphate (DPHP) is presently reported in embryonated eggs and chicks of Japanese quail. Quail were dosed with TPHP at 3 concentrations by air cell egg injection on embryonic day 0, followed by daily oral dosing after chicks hatched (5 d). Vehicle‐only exposed controls were also used. In dosed eggs, only 33% of the TPHP remained 2 d after injection (no hepatic development); after 10 d (post‐hepatogenesis), only 2% remained. The estimated TPHP half‐lives in the eggs ranged from 1.1 to 1.8 d for the 3 dosed groups. In all exposed eggs and chicks, DPHP significantly increased with dose (0.001 < p < 0.044). It appears that DPHP is an important metabolite in quail, making up 41 to 74% of all metabolites formed in embryonated eggs. In chicks, at medium and high doses, DPHP concentrations significantly exceeded those of TPHP (p ≤ 0.007), making up 67 and 76% of the total burden, respectively. Our findings suggest that rapid TPHP metabolism occurred in chicks and embryonated quail eggs but that this may vary with the age of the embryonated egg and the stage of embryo development, which should be considered when evaluating concentrations of TPHP and DPHP measured in eggs of wild birds. Environ Toxicol Chem 2020;39:565–573. © 2019 Her Majesty the Queen in Right of Canada. Environmental Toxicology and Chemistry © 2019 SETAC

Effects of Avian Eggshell Oiling With Diluted Bitumen Show Sublethal Embryonic Polycyclic Aromatic Compound Exposure

King

Elliott

Marlatt

et al. 2021

Breeding birds that become oiled may contaminate the shells of their eggs, and studies of conventional crude oil suggest that even small quantities can be absorbed through the eggshell and cause embryotoxicity. Unconventional crude oils remain untested, so we evaluated whether a major Canadian oil sands product, diluted bitumen (dilbit), would be absorbed and cause toxicity when applied to eggshells of two species, domestic chicken (Gallus gallus domesticus) and double-crested cormorant (Nannopterum auritum). We artificially incubated eggs and applied lightly weathered dilbit (Cold Lake blend) to the eggshells (0.015-0.15 mg g −1 egg in chicken; 0.1-0.4 mg g −1 egg in cormorant) at various points during incubation before sampling prehatch embryos. Polycyclic aromatic compound (PAC) residue in cormorant embryos was elevated only at the highest dilbit application (0.4 mg g −1 egg) closest (day 16) to sampling on day 22. In contrast, cormorant liver cytochrome P450 1a4 (Cyp1a4) mRNA expression (quantitative polymerase chain reaction assay) was elevated only in embryos treated with the earliest and lowest dilbit application (0.1 mg g −1 egg on day 4). These results confirm that dilbit can cross through the eggshell and be absorbed by embryos, and they imply rapid biotransformation of PACs and a nonmonotonic Cyp1a4 response. Despite evidence of exposure in cormorant, we found no detectable effects on the frequency of survival, deformity, and gross lesions, nor did we find effects on physiological endpoints indicative of growth and cardiovascular function in either chicken or cormorant. In ovo dilbit exposure may be less toxic than well-studied conventional crude oils. The effects of an oil spill scenario involving dilbit to bird embryos might be subtle, and PACs may be rapidly metabolized.