Larval Exposure to 4-Nonylphenol and 17-Estradiol Affects Physiological and Behavioral Development of Seawater Adapta
详细信息 查看全文
- 作者：Darren T. Lerner ; Bjö ; rn Thrandur Bjö ; rnsson ; Stephen D. McCormick
- 刊名：Environmental Science & Technology
- 出版年：2007
- 出版时间：June 15, 2007
- 年：2007
- 卷：41
- 期：12
- 页码：4479 - 4485
- 全文大小：187K
- 年卷期：v.41,no.12(June 15, 2007)
- ISSN：1520-5851
文摘
Population declines of anadromous salmonids areattributed to anthropogenic disturbances including dams,commercial and recreational fisheries, and pollutants, suchas estrogenic compounds. Nonylphenol (NP), a xenoestrogen, is widespread in the aquatic environment due to its usein agricultural, industrial, and household products. Weexposed Atlantic salmon yolk-sac larvae to waterborne 10or 100 
g L-1 NP (NP-L or NP-H, respectively), 2 g L-1 17
-estradiol (E2), or vehicle, for 21 days to investigate their effectson smolt physiology and behavior 1 year later. NP-Hcaused approximately 50% mortality during exposure, 30days after exposure, and 60 days after exposure. Mortalityrates of NP-L and E2 fish were not affected until 60 daysafter treatment, when they were 4-fold greater than those ofcontrols. Treatment with NP-L or E2 as yolk-sac larvaedecreased gill sodium-potassium-activated adenosinetriphosphatase (Na+,K+-ATPase) activity and seawater(SW) tolerance during smolt development, 1 year afterexposure. Exposure to NP-L and E2 resulted in a latencyto enter SW and reduced preference for SW approximately2- and 5-fold, respectively. NP-L-exposed fish had 20%lower plasma insulin-like growth factor I(IGF-I) levels and 35% lower plasma triiodothyronine (T3).Plasma growth hormone and thyroxine (T4) were unaffected.Exposure to E2 did not affect plasma levels of IGF-I, GH,T3, or T4. Both treatment groups exhibited increased plasmacortisol and decreased osmoregulatory capacity inresponse to a handling stressor. These results suggestthat early exposure to environmentally relevant concentrationsof NP, and other estrogenic compounds, can causedirect and delayed mortalities and that this exposure canhave long term, "organizational" effects on life-historyevents in salmonids.
g L-1 NP (NP-L or NP-H, respectively), 2 g L-1 17-estradiol (E2), or vehicle, for 21 days to investigate their effectson smolt physiology and behavior 1 year later. NP-Hcaused approximately 50% mortality during exposure, 30days after exposure, and 60 days after exposure. Mortalityrates of NP-L and E2 fish were not affected until 60 daysafter treatment, when they were 4-fold greater than those ofcontrols. Treatment with NP-L or E2 as yolk-sac larvaedecreased gill sodium-potassium-activated adenosinetriphosphatase (Na+,K+-ATPase) activity and seawater(SW) tolerance during smolt development, 1 year afterexposure. Exposure to NP-L and E2 resulted in a latencyto enter SW and reduced preference for SW approximately2- and 5-fold, respectively. NP-L-exposed fish had 20%lower plasma insulin-like growth factor I(IGF-I) levels and 35% lower plasma triiodothyronine (T3).Plasma growth hormone and thyroxine (T4) were unaffected.Exposure to E2 did not affect plasma levels of IGF-I, GH,T3, or T4. Both treatment groups exhibited increased plasmacortisol and decreased osmoregulatory capacity inresponse to a handling stressor. These results suggestthat early exposure to environmentally relevant concentrationsof NP, and other estrogenic compounds, can causedirect and delayed mortalities and that this exposure canhave long term, "organizational" effects on life-historyevents in salmonids.