Details zur Publikation

Referenztyp Zeitschriften
DOI / URL Link
Titel (primär) Special issue: zebrafish teratogenesis
Autor Scholz, S.;
Journal / Serie Reproductive Toxicology
Erscheinungsjahr 2012
Department BIOTOX;
Band/Volume 33
Heft 2
Sprache englisch;
Keywords Editorial; Zebrafish embryo; Screening; Alternatives to animal experiments; Teratogenic; Microarray
Abstract

The gulf toadfish (Opsanus beta) is unusual among teleosts in that it is facultatively ureotelic and adults and juveniles have a particularly high tolerance to environmental ammonia. Male toadfish brood their offspring in confined nests. It has been hypothesized that the potential accumulation of ammonia in nests from the male and the offspring, coupled with suspected low ammonia tolerance in offspring would provide the selective pressure necessary for excretion of the less toxic urea by adult toadfish. This study examines this so-called ‘nest-fouling’ hypothesis through acute and chronic ammonia toxicity testing on early life stages of O. beta. In addition, nitrogen elimination was examined among embryos, yolk-sac larvae and juveniles where we found an ontogenic shift from ammonotely to ureotely with advancing life history stages. The acute ammonia 96 h LC50 values for embryos and larvae were 63.6 and 5.45 mmol-N l−1 total ammonia (TAmm), respectively. Thus, these early life stages are more tolerant to ammonia than either juveniles or adults and LC50 values are at least 2 orders of magnitude greater than concentrations naturally occurring at nest sites. Furthermore, 40 days exposures at mean and maximum NH3 concentrations normally found within nests revealed no observable detrimental effects. In fact, growth in terms of wet or dry weight was greatest at the maximum NH3 concentration. We therefore conclude that the nest-fouling hypothesis is not a viable explanation for ureotely in the gulf toadfish.
ID 12286
dauerhafte UFZ-Verlinkung https://www.ufz.de/index.php?en=20939&ufzPublicationIdentifier=12286
Scholz, S. (2012):
Special issue: zebrafish teratogenesis
Reprod. Toxicol. 33 (2), 127 - 127