Is the gonadotropin releasing hormone system vulnerable to endocrine disruption in birds?

Abstract Endocrine disrupting chemicals (EDCs) from a variety of sources occur widely in the environment, but relationships between exposure to EDCs and long term effects on bird populations can be difficult to prove. Embryonic exposure to EDCs may be particularly detrimental, with potential long-te...

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Bibliographic Details
Published in:General and comparative endocrinology 2009-09, Vol.163 (1), p.104-108
Main Authors: Ottinger, Mary Ann, Lavoie, Emma T, Thompson, Nicola, Bohannon, Meredith, Dean, Karen, Quinn, Michael J
Format: Article
Language:English
Subjects:
Animals
Birds
Coturnix - embryology
Coturnix - metabolism
Coturnix - physiology
Coturnix japonica
Endocrine disrupting chemicals
Endocrine Disruptors - toxicity
Endocrinology & Metabolism
Gonadotropin releasing hormone-I
Gonadotropin-Releasing Hormone - metabolism
Hypothalamus - drug effects
Lifetime fitness
Reproduction - drug effects
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Summary:Abstract Endocrine disrupting chemicals (EDCs) from a variety of sources occur widely in the environment, but relationships between exposure to EDCs and long term effects on bird populations can be difficult to prove. Embryonic exposure to EDCs may be particularly detrimental, with potential long-term effects on reproduction and ultimately individual fitness. Because many EDCs may have subtle sublethal effects, it is necessary to establish sensitive end points as biomarkers of EDC exposure in birds. Because the effects of EDCs may be both short- and long-term, it is important to determine if embryonic exposure impacts sexual differentiation and development of the reproductive axis in hatchlings and if there are effects on reproductive function in adults. Our studies have focused on the effects of estrogen- and androgen-active EDCs on the hypothalamic gonadotropin releasing hormone–I (GnRH-I) system in an avian model of precocial species, the Japanese quail. Estrogen- or androgen-active EDCs were administered between 0 and embryonic day 4, and hypothalamic GnRH-I was measured in hatchlings and adults. Treatment with vinclozolin and PCB126 depressed the concentration of embryonic GnRH-I peptide while methoxyclor had an inconsistent stimulatory effect. Treatment with atrazine or trenbolone had no significant effects on hypothalamic GnRH-I in adults. Overall these observations support the view that the developing avian GnRH-I neural system may be vulnerable to EDCs with potential to alter lifelong reproductive function.
ISSN:0016-6480
1095-6840
DOI:10.1016/j.ygcen.2009.05.007