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Neuroendocrine Disruption By 17alpha-Ethinylestradiol and Bisphenol-A in Zebrafish.

Record Type:	Language materials, manuscript : Monograph/item
Title/Author:	Neuroendocrine Disruption By 17alpha-Ethinylestradiol and Bisphenol-A in Zebrafish./
Author:	Wooten, Taelah.
Description:	1 online resource (77 pages)
Notes:	Source: Masters Abstracts International, Volume: 57-01.
Subject:	Biology. -
Online resource:	click for full text (PQDT)
ISBN:	9780355285802

Neuroendocrine Disruption By 17alpha-Ethinylestradiol and Bisphenol-A in Zebrafish.
Wooten, Taelah.

Neuroendocrine Disruption By 17alpha-Ethinylestradiol and Bisphenol-A in Zebrafish. - 1 online resource (77 pages)

Source: Masters Abstracts International, Volume: 57-01.

Thesis (M.S.)--Texas A&M University - Commerce, 2017.

Includes bibliographical references

Aquatic organisms are highly susceptible to endocrine disruption due to increased accumulation of estrogenic endocrine disrupting chemicals (EDCs) in surface waters. The consequence of EDC exposure has not been well characterized in the adult male reproductive neuroendocrine system, although there is considerable circumstantial evidence for neuroendocrine disruption based on limited information available in the literature. This study was designed to evaluate the effects of environmental contaminants 17alpha-ethinylestradiol (EE2) and bisphenol-A (BPA) on adult male zebrafish reproduction. It was hypothesized that EE2 and BPA will act as estrogen mimics to inhibit the male hypothalamus-pituitary-gonadal (HPG) axis. In the first experiment, adult male zebrafish in three treatment groups were injected with 0.1, 1, or 10 nmol/kg EE2, once a week for three weeks. The control received sham injections. At the end of the three weeks, whole brain tissue samples were collected and analyzed for changes in Kisspeptin (Kiss) using a commercially purchased Kiss enzyme linked immunoassay kit. Gonadal samples were collected for evaluation of any histopathological changes in the testes and water samples, after immersing individual fish in 100 ml water for one hour, were collected to evaluate sex steroid production. A similar experiment was performed using 0.1,1, and 10 ?mol/kg BPA injections and the same neuroendocrine and reproductive parameters were evaluated after the 3-week exposure period.

Electronic reproduction.
Ann Arbor, Mich. :
ProQuest,
2018

Mode of access: World Wide Web

ISBN: 9780355285802Subjects--Topical Terms:

599573
Biology.
Index Terms--Genre/Form:

554714
Electronic books.

Neuroendocrine Disruption By 17alpha-Ethinylestradiol and Bisphenol-A in Zebrafish.
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500 $a Source: Masters Abstracts International, Volume: 57-01.
500 $a Adviser: Izhar Khan.
502 $a Thesis (M.S.)--Texas A&M University - Commerce, 2017.
504 $a Includes bibliographical references
520 $a Aquatic organisms are highly susceptible to endocrine disruption due to increased accumulation of estrogenic endocrine disrupting chemicals (EDCs) in surface waters. The consequence of EDC exposure has not been well characterized in the adult male reproductive neuroendocrine system, although there is considerable circumstantial evidence for neuroendocrine disruption based on limited information available in the literature. This study was designed to evaluate the effects of environmental contaminants 17alpha-ethinylestradiol (EE2) and bisphenol-A (BPA) on adult male zebrafish reproduction. It was hypothesized that EE2 and BPA will act as estrogen mimics to inhibit the male hypothalamus-pituitary-gonadal (HPG) axis. In the first experiment, adult male zebrafish in three treatment groups were injected with 0.1, 1, or 10 nmol/kg EE2, once a week for three weeks. The control received sham injections. At the end of the three weeks, whole brain tissue samples were collected and analyzed for changes in Kisspeptin (Kiss) using a commercially purchased Kiss enzyme linked immunoassay kit. Gonadal samples were collected for evaluation of any histopathological changes in the testes and water samples, after immersing individual fish in 100 ml water for one hour, were collected to evaluate sex steroid production. A similar experiment was performed using 0.1,1, and 10 ?mol/kg BPA injections and the same neuroendocrine and reproductive parameters were evaluated after the 3-week exposure period.
520 $a EE2 (10 nmol/kg) injections significantly increased Kiss content, decreased the size of the testes and inhibited production of sperm. However, EE2 did not significantly alter sex steroid levels. On the other hand, BPA (1 ?mol/kg) injections only decreased the density of mature sperm in the testes. BPA administrations did not significantly alter Kiss content or sex steroid levels. EE2 acted as an estrogen mimic to alter Kiss content; however, it produced a Kiss surge characteristic of the pre-ovulatory surge in female mammals (Kauffman, 2010; Okamuru et al., 2013; Rudolph et al., 2016). EE2 also inhibited spermatogenesis by inducing estrogen toxicity in the testes similar to what has been reported by Van der Ven et al. (2003). BPA exposure at the doses used in the present study induced non-significant alterations in Kiss peptide, testes histology, and sex steroid production in adult male zebrafish. Mechanisms of action of BPA on male reproductive axis may involve non-estrogenic pathways because it did not produce the same changes in the HPG axis as seen with EE2. Results of this study show that the two estrogenic EDCs, EE2 and BPA, can act at multiple levels of the HPG axis to disrupt male reproductive system. Kisspeptin neurons in the brain appear to be an important target of neuroendocrine disruption by environmental xenoestrogens resulting in the impairment of vertebrate reproduction.
533 $a Electronic reproduction. $b Ann Arbor, Mich. : $c ProQuest, $d 2018
538 $a Mode of access: World Wide Web
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650 4 $a Endocrinology. $3 645497
650 4 $a Toxicology. $3 580973
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