Xenoestrogenic effects of ethinylestradiol in zebrafish (<i>Danio rerio</i>)

Versonnen, Bram; Janssen, Colin R.

doi:10.1002/tox.20012

Cited by 65 publications

(33 citation statements)

References 45 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…There was no change in levels of expression between treatment or timepoints in the female fish. In the male fish there was no significant difference in expression between the control and the QUIN group, however the males exposed to EE 2 demonstrated significantly higher levels of expression, which is consistent with results from other studies (Versonnen & Janssen, 2004).…”

Section: Estrogenicitysupporting

confidence: 91%

“…The effect of EE 2 exposure on fish fecundity has been well documented (Rahman, Yanful, & Jasim, 2009;Segner et al, 2003). EE 2 exposure results in reduced ovary size, altered gonadal structure ( Van den Belt, et al, 2002;Versonnen & Janssen, 2004) and a decline in expression of genes involved in the follicular recruitment and steroidogenesis, maturation and ovulation pathways (Carnevali et al, 2010;Urbatzka et al, 2012;Van den Belt et al, 2001). …”

Section: Thesis Objectives and Outlinementioning

confidence: 99%

“…; Van den Belt, et al, 2002;Versonnen & Janssen, 2004). Generally, the major fraction of ovarian volume is made up of the larger later stage follicles, a lack of these follicle stages in the ovaries of the EE 2 fish could explain the decreased GSI observed.…”

mentioning

confidence: 99%

See 2 more Smart Citations

Inhibition of spawning in zebrafish (Danio rerio): Adverse outcome pathways of quinacrine and ethinylestradiol

Cosme

Lister

Kraak

2015

General and Comparative Endocrinology

View full text Add to dashboard Cite

INHIBITION OF SPAWNING IN ZEBRAFISH (Danio rerio): ADVERSE OUTCOME PATHWAYS OF QUINACRINE AND ETHINYLESTRADIOL Madelyne CosmeAdvisor: University of Guelph, 2014Professor. Glen Van Der KraakThis study examined the effects of estrogen receptor agonist, ethinylestradiol, and the phospholipase A 2 inhibitor, quinacrine, on the pathways controlling follicular recruitment, steroidogenesis, oocyte maturation and ovulation and spawning success in the adult zebrafish. Ethinylestradiol and quinacrine both inhibit spawning but did so through different adverse outcome pathways. Ethinylestradiol affected follicular recruitment (reduced ovarian size and reduction in the proportion of cortical alveolus, vitellogenic and mature follicle stages), steroidogenesis (reduced expression of aromatase) maturation (reduced luteinizing hormone receptor expression) and ovulation (reduced expression of cytosolic phospholipase A2 and the nuclear progesterone receptor). Quinacrine targeted ovulation via a reduction of the steroid 17α, 20β dihydroxy-4-prenen-3-one and expression of the prostaglandin metabolizing enzyme cyclooxygenase 2. Collectively, these studies suggest that a targeted assessment of reproductive endpoints can be used effectively to identify the adverse outcome pathways by which toxicants can impact reproductive fitness.iii ACKNOWLEDGEMENTS

show abstract

Section: Estrogenicitysupporting

confidence: 91%

Section: Thesis Objectives and Outlinementioning

confidence: 99%

See 1 more Smart Citation

Inhibition of spawning in zebrafish (Danio rerio): Adverse outcome pathways of quinacrine and ethinylestradiol

Cosme

Lister

Kraak

2015

General and Comparative Endocrinology

View full text Add to dashboard Cite

show abstract

“…Animals exposed to environmental estrogens have exhibited defects in sexual development, sexual behavior, and reproduction organ malformation (Blomqvist et al 2006, Furuya et al 2006, Ma & Sassoon 2006. Besides these effects, fishes display abnormal intersexuality, reduced spawning success, reduced female fecundity, delayed male gonadal differentiation, reproductive duct malformation, and complete sex reversal (Jobling et al 1998, Scholz & Gutzeit 2000, Van den Belt et al 2001, Balch et al 2004, Nash et al 2004, Versonnen & Janssen 2004, Mills & Chichester 2005, Campbell et al 2006.…”

Section: Introductionmentioning

confidence: 99%

Reduced embryonic survival in rainbow trout resulting from paternal exposure to the environmental estrogen 17α-ethynylestradiol during late sexual maturation

Brown¹,

Schultz²,

Nagler³

2007

Reproduction

View full text Add to dashboard Cite

Exposure of fishes to environmental estrogens is known to affect sexual development and spawning, but little information exists regarding effects on gametes. This study evaluated embryonic survival of offspring from male rainbow trout (Oncorhynchus mykiss) exposed to 17a-ethynylestradiol (EE 2 ) using an in vitro fertilization protocol. Males were exposed at either 1800 or 6700 degree days (8d) (i.e. 161 or 587 days post-fertilization (dpf)) to test for effects on testes linked to reproductive ontogeny. At 18008d, fish were beginning testicular differentiation and were exposed to 109 ng EE 2 /l for 21 days. At 67008d, fish have testes containing spermatocytes and spermatids and were exposed for 56 days to either 0.8, 8.3, or 65 ng EE 2 /l. Semen was collected at full sexual maturity in each group and used to fertilize eggs pooled from several non-exposed females. Significant decreases in embryonic survival were observed only with the 67008d exposure. In 0.8 and 8.3 ng EE 2 /l treatments, embryo survival was significantly reduced at 19 dpf when compared with the control. In contrast, an immediate decrease in embryonic survival at 0.5 dpf was observed in the 65 ng EE 2 /l treatment. Blood samples collected at spawning from 67008d exposed males revealed a significant decrease in 11-ketotestosterone and a significant increase in luteinizing hormone levels for the 65 ng EE 2 /l treatment when compared with the other treatment groups. Results indicate that sexually maturing male rainbow trout are susceptible to EE 2 exposure with these fish exhibiting two possible mechanisms of reduced embryonic survival through sperm varying dependant on EE 2 exposure concentrations experienced.

show abstract

“…Indeed, laboratory-based studies have shown that some environmental oestrogens not only affect reproduction of fish but can also impact on other endocrinemediated processes, including somatic growth (e.g. 17a-ethinyloestradiol (EE 2 ; Versonnen & Janssen 2004, Van den Belt et al 2003, 4-tert-nonylphenol (NP; Dreze et al 2000, Magliulo et al 2002, methoxychlor (Magliulo et al 2002)), osmoregulation (e.g. 17b-oestradiol (E 2 ) and NP (Madsen et al 1997, Vijayan et al 2001, Arsenault et al 2004, Madsen et al 2004, McCormick et al 2005), immune function (e.g.…”

Section: Introductionmentioning

confidence: 99%

Multiple molecular effect pathways of an environmental oestrogen in fish

Filby¹,

Thorpe²,

Tyler³

2006

Journal of Molecular Endocrinology

130

View full text Add to dashboard Cite

Complex interrelationships in the signalling of oestrogenic effects mean that environmental oestrogens present in the aquatic environment have the potential to disrupt physiological function in fish in a more complex manner than portrayed in the present literature. Taking a broader approach to investigate the possible effect pathways and the likely consequences of environmental oestrogen exposure in fish, the effects of 17b-oestradiol (E 2 ) were studied on the expression of a suite of genes which interact to mediate growth, development and thyroid and interrenal function (growth hormone GH (gh), GH receptor (ghr ), insulin-like growth factor (IGF-I) (igf1), IGF-I receptor (igf1r ), thyroid hormone receptors-a (thra) and -b (thrb) and glucocorticoid receptor (gr )) together with the expression analyses of sex-steroid receptors and ten other genes centrally involved in sexual development and reproduction in fathead minnow (fhm; Pimephales promelas). Exposure of adult fhm to 35 ng E 2 /l for 14 days induced classic oestrogen biomarker responses (hepatic oestrogen receptor 1 and plasma vitellogenin), and impacted on the reproductive axis, feminising 'male' steroidogenic enzyme expression profiles and suppressing genes involved in testis differentiation. However, E 2 also triggered a cascade of responses for gh, ghr, igf1, igf1r, thra, thrb and gr in the pituitary, brain, liver, gonad and gill, with potential consequences for the functioning of many physiological processes, not just reproduction. Molecular responses to E 2 were complex, with most genes showing differential responses between tissues and sexes. For example, igf1 expression increased in brain but decreased in gill on exposure to E 2 , and responded in an opposite way in males compared with females in liver, gonad and pituitary. These findings demonstrate the importance of developing a deeper understanding of the endocrine interactions for unravelling the mechanisms of environmental oestrogen action and predicting the likely health consequences.

show abstract

Xenoestrogenic effects of ethinylestradiol in zebrafish (Danio rerio)

Cited by 65 publications

References 45 publications

Inhibition of spawning in zebrafish (Danio rerio): Adverse outcome pathways of quinacrine and ethinylestradiol

Inhibition of spawning in zebrafish (Danio rerio): Adverse outcome pathways of quinacrine and ethinylestradiol

Reduced embryonic survival in rainbow trout resulting from paternal exposure to the environmental estrogen 17α-ethynylestradiol during late sexual maturation

Multiple molecular effect pathways of an environmental oestrogen in fish

Contact Info

Product

Resources

About