| one publication added to basket [102829] | Laboratory exposure to 17ß-estradiol fails to induce vitellogenin and estrogen receptor gene expression in the marine invertebrate Mytilus edulis
Puinean, A.M.; Labadie, P.; Hill, E.M.; Osada, M.; Kishida, M.; Nakao, R.; Novillo, A.; Callard, I.P.; Rotchell, J.M. (2006). Laboratory exposure to 17ß-estradiol fails to induce vitellogenin and estrogen receptor gene expression in the marine invertebrate Mytilus edulis. Aquat. Toxicol. 79(4): 376-383. http://dx.doi.org/10.1016/j.aquatox.2006.07.006
In: Aquatic Toxicology. Elsevier Science: Tokyo; New York; London; Amsterdam. ISSN 0166-445X; e-ISSN 1879-1514, more
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| Keywords |
Biomarkers
Cultures > Shellfish culture > Mollusc culture > Mussel culture
Vitellogenesis
Mytilus edulis Linnaeus, 1758 [WoRMS]
Marine/Coastal |
| Author keywords |
vitellogenin; mussel; endocrine disruption; biomarker |
| Authors | | Top |
- Puinean, A.M.
- Labadie, P.
- Hill, E.M.
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- Osada, M.
- Kishida, M.
- Nakao, R.
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- Novillo, A.
- Callard, I.P.
- Rotchell, J.M.
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| Abstract |
To investigate the effect of estrogenic compounds on the marine mussel Mytilus edulis, an assay was developed to measure the expression of two vertebrate estrogen responsive genes—estrogen receptor (ER) and vitellogenin (VTG) genes. Expression was measured in M. edulis gonads following a 10-day exposure to 200 ng/l 17β-estradiol (estradiol). The concentrations of esterified estradiol in mussel tissue increased 15-fold in a time-dependent manner—confirming uptake of the compound by the mussels, however there was no significant increase of free estradiol in mussel tissues during the exposure period. The ER and VTG mRNA levels in the gonads of both sexes were measured at days 1–3, 5, and 10 in control and exposed mussels. However, no significant change in the expression of either the ER or VTG genes was recorded at any of the sampled time points. The results suggest that either a regulatory mechanism exists in a mussel that is able to maintain constant levels of free estradiol by converting the excess estradiol into esterified products which may have reduced affinity for the estrogen receptor, or alternatively, that the ER and VTG genes are unresponsive to estrogens in these organisms. The significance of these findings in terms of the utility of ER and VTG as biomarkers of endocrine disruption in bivalve species is discussed. |
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