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Grantee Research Project Results

NCER Grantee Research Project Results

Effects of Environmental Endocrine Disruptors on Growth in the Tilapia

EPA Grant Number: FP916428
Title: Effects of Environmental Endocrine Disruptors on Growth in the Tilapia
Investigators: Berg, Lori K.
Institution: University of Hawaii at Manoa
EPA Project Officer: Manty, Dale
Project Period: January 1, 2004 through December 31, 2006
Project Amount: $88,288
RFA: STAR Graduate Fellowships (2004)
Research Category: Academic Fellowships , Biology/Life Sciences , Fellowship - Biochemistry, Molecular Biology, Cell Biology, Development Biology, and Genetics

Description:

Objective:

Environmental endocrine disruptors (EEDs) are manmade compounds that alter many aspects of animal physiology, most notably reproduction and development. To date, however, few studies have been done on the effects of EEDs on growth regulation. In vertebrates in general, growth hormone (GH ), released from the pituitary gland, stimulates somatic growth by either acting directly on tissues or indirectly by acting through its mediator, insulin-like growth factor-I (IGF-I ). IGF-I actions are regulated tightly by the IGF-binding protein (IGFBP) family. The objective of my research is to determine how several classes of EEDs alter the GH-IGF-I axis in a euryhaline teleost, the tilapia (Oreochromis mossambicus). I hypothesize that EEDs suppress the GH-IGF-I axis, in part by upregulating production of the egg yolk precursor protein vitellogenin (VTG).

Approach:

To test my hypothesis, I will conduct both in vitro and in vivo studies. For in vitro studies , I will use primary cultures of hepatocytes and pituitary glands prepared from male and female tilapia, in which cells will be exposed to EEDs . After various periods of incubation, the hepatocyte culture medium will be analyzed for VTG and IGFBPs released into the medium. Hepatocyte mRNA will be analyzed for the expression of IGF-I, VTG, and GH and estrogen receptors (GH-R, E2-αR, E2-βR, respectively). Pituitary culture medium will be analyzed for secreted GH, and tissue will be collected to analyze expression of GH, IGF-I, E2-αR, and E2-βR. In vivo studies will be performed on male and female tilapia of various ages to examine the presence of sex and/or age-specific differences. Tilapia will be injected with various EEDs , and the plasma sample s will be taken weekly for 1 month. Plasma will be analyzed for levels of GH, IGF-I, IGFBPs, and VTG. On the last sampling time point , various tissues will be removed for examination of mRNA expression: liver (IGF-I, VTG, E2-αR, E2-βR, GH-R), gonads (IGF-I, E2-αR, E2-βR), and pituitary (GH, E2-αR, E2-βR). These studies will provide a new insight into the mechanism of action of EED on growth regulation not only in fish but also in vertebrates in general.

Supplemental Keywords:

fellowship, environmental endocrine disruptors, telost, tilapia, growth hormone, mRNA expression, growth regulation,, RFA, Health, Scientific Discipline, POLLUTANTS/TOXICS, Environmental Chemistry, Health Risk Assessment, Chemicals, Endocrine Disruptors - Environmental Exposure & Risk, endocrine disruptors, Risk Assessments, Biochemistry, Biology, Endocrine Disruptors - Human Health, bioindicator, assays, biomarkers, growth hormone, EDCs, endocrine disrupting chemicals, exposure studies, sexual development, human growth and development, toxicity, endocrine disrupting chemcials, estrogen response, Tilapia, invertebrates, invertebrate model, hormone production, androgen, estrogen receptors, ecological risk assessment model, assessment technology, estuarine crustaceans

Relevant Websites:

2004 STAR Graduate Fellowship Conference Poster (PDF, 1p., 148KB, about PDF)

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The perspectives, information and conclusions conveyed in research project abstracts, progress reports, final reports, journal abstracts and journal publications convey the viewpoints of the principal investigator and may not represent the views and policies of ORD and EPA. Conclusions drawn by the principal investigators have not been reviewed by the Agency.

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