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KMID : 1025520090510060485
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Journal of Animal Science and Technology
2009 Volume.51 No. 6 p.485 ~ p.492
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Physiological Effects of Diethylstilbestrol Exposure on the Development of the Chicken Oviduct.
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Seo Hee-Won
Park Kyung-Je
Lee Hyung-Chul
Kim Dae-Yong
Song Yong-Sang
Lim Jeong-Mook
Song Gwon-Hwa
Han Jae-Yong
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Abstract
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Estrogen has dramatic effects on the development and function of the reproductive tract in mammals. Although diethylstilbestrol (DES) triggers the development of reproductive organs in immature animals, continued exposure to DES induces dysfunction of the female reproductive tract in mice. To investigate the effects of neonatal estrogen exposure on the reproductive tract of female chickens, we implanted DES pellets into the abdominal region of immature female chicks and then examined the effects of DES on the oviducts of both immature chicks and sexually mature chickens(30 weeks old). DES induced mass growth and differentiation of the oviduct in immature chicks. The chick oviduct increased by 2.7- and 29-fold in length and weight, respectively, following primary DES stimulation. In secondary DES stimulation, the length and weight of the chick oviduct increased by 4.5- and 74-fold, respectively. Additionally, DES treatments caused abnormal development of the infundibulum and magnum in hen oviducts. Furthermore, infundibulum abnormality gave rise to unusual ovulation of follicles and resulted in infertility and dysfunction of the magnum, such as less production of egg white proteins. Our results indicate that DES exposure during early developmental stages in chickens has detrimental effects on the development and maintenance of the female reproductive tract after sexual maturation.
Steroid hormones are major modulators of the development of the female reproductive system. Estrogen, the primary female sex hormone, is mainly secreted by granulosa cells of preovulatory follicles under the regulation of gonadotrophin in humans and mice(McNatty et al., 1979; Voronina et al., 2007). Estrogen also regulates the proliferation and differentiation of germ cells, induces the development of female reproductive organs, including the uterus and oviduct, and influences pregnancy in mammals (De Pol et al., 2001; Hewitt et al., 2005; Jefferson et al., 2006).
In chickens, estrogen regulates the ovulatory cycle and production of egg white proteins. The peak of estradiol concentration in laying hens is related to ovulation and ovoposition(Lague et al., 1975), and estrogen treatment increases the expression of egg white proteins such as ovalbumin(Oka and Schimke, 1969). Estrogen also influences the sexual differentiation of unspecialized gonads during chicken embryo development, and estrogen receptors are expressed in the medulla of both gonads and the germinal epithelium. However, the role of estrogen in the sexual differentiation process is considered a neutral factor and not an origin of sex differences(Gasc, 1980). However, administration of estrogen affects the development of immature chick oviducts(Kohler et al., 1969). Not only does estrogen trigger cell proliferation and differentiation of the chick oviduct, but also prevents cellular apoptosis. For example, oviduct weight increases by up to 1.5 g following estrogen stimulation during the 2 weeks after birth(Palmiter and Wrenn, 1971). Epithelial cells in the chicken oviduct differentiate into tubular gland cells, goblet cells, and ciliated cells in response to estrogen (Kohler et al., 1969). Also, the removal of estrogen treatment results in sharply increased cell death in the oviduct and increased expression of genes related to apoptosis, such as the caspase gene family(Monroe et al., 2000; Monroe et al., 2002).
Estrogen analogs have been used to examine the functions of estrogen in the mammalian reproductive tract and for medical applications. One estrogen analog is diethylstilbestrol (DES), which is a synthetic non-steroidal compound. Because DES has activity similar to estrogen, exposure to DES in immature chicks induces mass growth and differentiation of the chick oviduct, and rapidly increases the expression of egg white genes such as ovalbumin and lysozyme(Oka and Schimke, 1969). Furthermore, DES was medically utilized to prevent consecutive miscarriages from the late 1940s through the 1970s(Newbold, 2004). However, the medical application of DES was based on incomplete scientific information. Because the nature and function of DES are not wholly the same as those of natural estrogen, DES treatment unexpectedly caused harmful effects on the development of the female reproductive system and pregnant women. Perinatal exposure to DES induced structural malformation of the reproductive tract and paraovarian cysts of mesonephric origin(Newbold, 2004). As exposure to DES changes the genetic status of the developing uterus, it induces abnormal cytodifferentiation in the uterus(Huang et al., 2005).
In chickens, DES has been used to elucidate the mechanisms of oviduct development influenced by estrogen, to culture tubular gland cells from the chicken oviduct in vitro, and to study regulatory mechanisms of the chicken ovalbumin gene (Dougherty and Sanders, 2005). However, detrimental effects of DES on the chicken female reproductive system have not been clearly revealed. In this study, we evaluated the effects of DES on the development and function of the oviduct in neonatal(1-week-old) chicks and sexually matured chickens. We found that neonatal exposure to DES stimulated the growth and differentiation of neonatal chick oviducts; however, DES induced dysfunction of the adult chicken oviduct after sexual maturation and caused hen infertility.
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KEYWORD
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Chicken, Diethylstilbestrol, Estrogen, Oviduct
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