Shelby L. Steele

TL;DR: It is proposed that the induction of glutamine synthetase genes early in development and the subsequent formation of the active protein are preparatory for the increased capacity of the embryo to convert the toxic nitrogen end product, ammonia, into glutamine, which may then be utilized in the ornithine-urea cycle or other pathways.

TL;DR: Findings indicate that all four GSase isoforms are constitutively expressed in trout brain and are inducible under high external ammonia conditions, and elevation of GSase activities in fore-, mid- and hindbrain in response to environmental ammonia underlines the importance of brain GSase in the ammonia-stress response.

TL;DR: The data indicate that trout embryos have an efficient system to prevent ammonia accumulation in embryonic tissue, by conversion of ammonia to urea in embryonic tissues and through elevation of ammonia levels in the yolk.

TL;DR: Data suggest that a functional OUC may be present in the skeletal muscle tissues of R. erinacea and that enhanced urea excretion rates and the downregulation of the anchor OUC enzyme, arginase, in the liver may be critical in regulating tissue urea content under dilute‐seawater stress.

TL;DR: The results of this study suggest it is unlikely that the adaptive significance of ureotelism in toadfish is a means to prevent fouling nests with ammonia and in turn poisoning offspring; however, additional study is warranted.