期刊
AQUATIC TOXICOLOGY
卷 162, 期 -, 页码 66-72出版社
ELSEVIER SCIENCE BV
DOI: 10.1016/j.aquatox.2015.03.005
关键词
Bifenthin; Dopamine; 17 beta-estradiol (E2); Gonadotropin releasing hormone
资金
- University of California, Riverside, Agricultural Experiment Station Resource Allocation Program
Bifenthrin is a type I pyrethroid pesticide, which has been shown to increase plasma estrogen concentrations in several fish models. The mechanism of action by which bifenthrin alters 17 beta-estradiol (E2) is unclear. E2 biosynthesis is regulated through pituitary follicle stimulating hormone, which is directly controlled by hypothalamic gonadotropin releasing hormone (GnRH2). Since dopaminergic signaling significantly influences GnRH2 release in fish, the goal of the study was to determine the effect of a 96 hand 2 weeks exposure to bifenthrin on dopaminergic signaling in juvenile rainbow trout (Oncorhynchus mykiss) (RT). Our results indicated that a decrease in dopamine receptor 2A (DR2A) expression was associated with a trend toward an increase in plasma E2 following exposure at 96 h and 2 weeks, and a significant increase in the relative expression of vitellogenin mRNA at 2 weeks. DR2A mRNA expression decreased 426-fold at 96 h and 269-fold at 2 weeks in the brains of 1.5 ppb (3.55 pM) bifenthrin treated RT. There was an increase in tyrosine hydroxylase transcript levels at 96 h, which is indicative of dopamine production in the brains of the 1.5 ppb (3.55 pM) bifenthrin treated RT. A significant increase in the relative expression of GnRH2 was observed at 96 h but a significant decrease was noted after 2 weeks exposure indicating potential feedback loop activation. These results indicate that the estrogenic-effects of bifenthrin may result in part from changes in signaling within the dopaminergic pathway, but that other feedback pathways may also be involved. (C) 2015 Elsevier B.V. All rights reserved.
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