Z. Billinghurst et al., Effects of 4-n-nonylphenol and 17 beta-oestradiol on early development of the barnacle Elminius modestus, J EXP MAR B, 257(2), 2001, pp. 255-268
Citations number
56
Categorie Soggetti
Aquatic Sciences
Journal title
JOURNAL OF EXPERIMENTAL MARINE BIOLOGY AND ECOLOGY
Pollutants that are present in the aquatic environment and cause abnormal e
ndocrine function in wildlife populations have been termed endocrine disrup
ting chemicals (EDCs). The impacts of these chemicals on the reproduction a
nd development of vertebrates has been shown to be significant in both fiel
d studies and laboratory experiments. Over the past decade the number of in
vestigations into the impacts of EDCs that affect reproductive and sexual c
haracteristics (reproductive EDCs) has increased and evidence of their pote
ncy is evident in numerous wildlife species and through data from in vitro
tests. However, little information is available on whether chemicals which
act as EDCs in vertebrate species affect aquatic invertebrates. The case of
imposer in archeogastropods following exposure to tributyltin (TBT) is a n
otable exception. Moreover, a number of studies have shown that development
, fecundity and reproductive output of some aquatic invertebrates are affec
ted significantly by exposure to pollutants. In order to determine whether
external signs of exposure to vertebrate EDCs can be observed and monitored
in invertebrate species, we exposed larvae of the barnacle Elminius modest
us to environmentally realistic concentrations of the xeno-oestrogen, 4-n-n
onylphenol (NP), and the natural oestrogen, 17 beta -oestradiol (E-2). Earl
y life stages (nauplii and cyprids) were also exposed in the laboratory to
determine whether there were effects on the timing of larval development an
d settlement. Ovary development and size of juveniles was measured followin
g chronic exposure. Exposure to NP in the concentration range 0.01-10 mug l
(-1) resulted in disruption of the timing of larval development. Similar re
sults were obtained with E-2. Pulse exposures showed that the timing of exp
osure is critical and exposures for a period of 12 months caused long-term
effects. A linear, concentration-dependent response was not evident. (C) 20
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