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ANALYSIS OF CHANGES IN GENE EXPRESSION PATTERNS IN FISH EXPOSED TO NATURAL PHARMACEUTICAL AND ENVIRONMENTAL ESTROGENS USING GENE ARRAYS.
Citation:
Denslow, N, P. Larkin, T. SaboAttwood, J. Kocerha, M J. Hemmer, AND L C. Folmar. ANALYSIS OF CHANGES IN GENE EXPRESSION PATTERNS IN FISH EXPOSED TO NATURAL PHARMACEUTICAL AND ENVIRONMENTAL ESTROGENS USING GENE ARRAYS. PRIMO - 12th Internat'l Symposium, Tampa, Fl, May 9-13, 2003.
Description:
Denslow, N.D., P. Larkin, T.L. Sabo-Attwood, J. Kocerha, K.J. Kroll, M.J. Hemmer and L.C. Folmar. 2004. Analysis of Changes in Gene Expression Patterns in Fish Exposed to Natural, Pharmaceutical and Environmental Estrogens Using Gene Arrays (Abstract). Mar. Environ. Res. 58(2-5):579-580. (ERL,GB R937).
Estrogen and estrogen-like contaminants disrupt the endocrine system of fish by binding to estrogen receptors and activating the estrogen-receptor mediated gene transcription pathway at inappropriate times. The genes that are activated are those involved in normal reproduction, normally responding to endogenous steroid hormones. These genes include vitellogenins, choriogenins, aspartic protease, and estrogen receptor, among others. Male largemouth bass injected IP with vehicle control (ethanol/DMSO diluent), 2.5 mg/kg 17 b-estradiol (E2), 50 mg/kg p-nonylphenol (NP) or 100 mg/kg p,p'-DDE were monitored for changes in gene expression using gene arrays. All of the compounds increased the expression of the same set of genes. In addition to the estrogen-like response, NP and DDE displayed unique gene expression profiles. In a second experiment, sheepshead minnows were treated with 65.1 ng/L E2 109 ng/L 17 a-ethynyl estradiol (EE2), 100 ng/L diethyl-stilbestrol, 11.8 ?g/L pNP, 590 ng/L endosulfan (ES), 5.6 ?g/L methoxychlor (MXC), or triethylene glycol (vehicle control) in a flow-through aqueous exposure system. In sheepshead minnows E2, DES, EE2, NP and MXC have similar genetic signatures for the 30 genes examined, but NP also showed up-regulation of ubiquitin-conjugating enzyme 9. ES did not up-regulate the same set of genes, with the exception of estrogen receptor a. It also specifically down-regulated 3-hydroxy-3-methylglutaryl CoA reductase. The responses obtained for EE2 were dose-dependent, in the range from 20 to 1000 ng/L, nominal concentrations. Overall, this research indicates that a better understanding of the consequences of exposure to endocrine disrupting compounds can be obtained from simultaneous monitoring of multiple genes.