Effects of estrogens and estrogenic disrupting compounds on fish mineralized tissues. | - CCMAR -

Journal Article

TítuloEffects of estrogens and estrogenic disrupting compounds on fish mineralized tissues.
Publication TypeJournal Article
AuthorsPinto, PIS, Estêvão, MD, Power, DM
Year of Publication2014
JournalMar Drugs
Volume12
Questão8
Date Published2014 Aug 15
Pagination4474-94
ISSN1660-3397
Palavras-chaveAnimals, Endocrine Disruptors, Estrogens, Fishes, Humans, Minerals, Protein Isoforms, Receptors, Estrogen, Reproduction
Abstract

Estrogens play well-recognized roles in reproduction across vertebrates, but also intervene in a wide range of other physiological processes, including mineral homeostasis. Classical actions are triggered when estrogens bind and activate intracellular estrogen receptors (ERs), regulating the transcription of responsive genes, but rapid non-genomic actions initiated by binding to plasma membrane receptors were recently described. A wide range of structurally diverse compounds from natural and anthropogenic sources have been shown to interact with and disrupt the normal functions of the estrogen system, and fish are particularly vulnerable to endocrine disruption, as these compounds are frequently discharged or run-off into waterways. The effect of estrogen disruptors in fish has mainly been assessed in relation to reproductive endpoints, and relatively little attention has been given to other disruptive actions. This review will overview the actions of estrogens in fish, including ER isoforms, their expression, structure and mechanisms of action. The estrogen functions will be considered in relation to mineral homeostasis and actions on mineralized tissues. The impact of estrogenic endocrine disrupting compounds on fish mineralized tissues will be reviewed, and the potential adverse outcomes of exposure to such compounds will be discussed. Current lacunae in knowledge are highlighted along with future research priorities.

DOI10.3390/md12084474
Sapientia

http://www.ncbi.nlm.nih.gov/pubmed/25196834?dopt=Abstract

Alternate JournalMar Drugs
PubMed ID25196834
PubMed Central IDPMC4145326
CCMAR Authors