Certain anthropogenic chemicals, most notably xeno-oestrogens, are known to have the potential to disrupt vertebrate endocrine systems. For example, induction of the female-specific protein, vitellogenin, in male fish is a well-known effect of exposure to xeno-oestrogens and serves as a biomarker of such exposure. There have been few comparable studies of putative biomarkers of endocrine disruption in invertebrates. An exception is the upregulation of vitellin-like larval storage protein (LSP) expression in the barnacle cypris larva following exposure to oestrogenic chemicals. The current study aimed to establish whether larvae of the glass prawn, Palaemon elegans, are likewise susceptible to xeno-oestrogen exposure. Using a polyclonal antiserum to P. elegans apolipovitellin, an 86 kDa polypeptide was detected by western blotting in the larval and early postlarval stages of this species. An indirect ELISA applied to the soluble protein fraction of larval homogenates determined that the titre of this putative LSP ranged, depending on larval stage, from 0.48–0.67 ng μg−1. Exposure of P. elegans larvae to the xeno-oestrogen 4-n-nonylphenol (4-NP), at 0.2–20 μg L−1, resulted in a significant, concentration-independent increase in putative LSP levels of 5–18%. Conversely, exposure to the natural oestrogen, 17β-oestradiol (E2), at 0.2 and 20 μg L−1, led to a significant concentration-independent decline (up to 11%) in LSP levels. Whether the effect of 4-NP results from endocrine disruption is not known, however, an oestrogen receptor-mediated effect is unlikely. Other than a slight increase in larval mortality when exposed to 4-NP at 2 μg L−1, neither 4-NP nor E2 significantly affected development, growth or survival of P. elegans larvae.
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1 January 2005
Larval Development and Vitellin-like Protein Expression in Palaemon elegans Larvae Following Xeno-oestrogen Exposure
Matthew B. Sanders,
Zoe Billinghurst,
Michael H. Depledge,
Anthony S. Clare
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Integrative and Comparative Biology
Vol. 45 • No. 1
January 2005
Vol. 45 • No. 1
January 2005