Environmental cues influence EDC-mediated endocrine disruption effects in different developmental stages of Japanese medaka (Oryzias latipes).
Temperature and photoperiod are the two most important environmental cues in the regulation of the annual cycles of circulating sex steroid hormones and reproduction in fish. Thus, these variables may alter the endocrine disruption effects induced by environmental endocrine disrupting chemicals (EDCs). In the present study, we found that the temperature and photoperiod significantly influence the transcription of the estrogen-responsive genes, vitellogenin1 (Vtg1), vitellogenin2 (Vtg2) and estrogen receptor-α (ERα) after a 7-day exposure to environmentally relevant concentrations of 17β-estradiol (E2) and nonylphenol (NP) in different developmental stages of Japanese medaka. In general, gene transcription levels increased as temperature and photoperiod length increased. The Vtg1 mRNA levels in 20 °C-12L group were 10-30 times higher than those in 10 °C-10 L group when larvae, both sexes of juvenile or male adult medaka were exposed to 50 ng/L E2. In addition, juveniles of both sexes and adult males were more sensitive to temperature and photoperiod changes than larval and adult female medaka. Specifically, two-way analysis indicated that both E2 and NP-mediated induction of Vtg1 mRNA (the most effective) expression interacted with environmental cues (temperature and photoperiod) and exposure concentrations in a developmental stage- and sex-specific manner. The results obtained in the present study demonstrate that the endocrine disrupting effects of environmental chemicals can be modified by seasonality and life stage in which the exposure occurs and that Vtg1 transcription is a good biomarker to evaluate these interactions.
College of Biological and Environmental Engineering, Zhejiang University of Technology, Hangzhou, China.
Yuanxiang
Y
Jin
Linjun
L
Shu
Feiyan
F
Huang
Limin
L
Cao
Liwei
L
Sun
Zhengwei
Z
Fu
D000367:Age Factors; D000704:Analysis of Variance; D000818:Animals; D017931:DNA Primers / Q000235:genetics; D052244:Endocrine Disruptors / Q000378:metabolism* / Q000633:toxicity; D004958:Estradiol / Q000378:metabolism / Q000633:toxicity; D047628:Estrogen Receptor alpha / Q000378:metabolism; D005786:Gene Expression Regulation / Q000502:physiology*; D012739:Gonadal Steroid Hormones / Q000097:blood*; D007814:Larva / Q000378:metabolism; D009990:Oryzias / Q000254:growth & development / Q000378:metabolism*; D010636:Phenols / Q000378:metabolism / Q000633:toxicity; D017440:Photoperiod; D012098:Reproduction / Q000187:drug effects* / Q000502:physiology; D020133:Reverse Transcriptase Polymerase Chain Reaction; D013696:Temperature; D014819:Vitellogenins / Q000378:metabolism
D017931:DNA Primers; D052244:Endocrine Disruptors; D047628:Estrogen Receptor alpha; D012739:Gonadal Steroid Hormones; D010636:Phenols; D014819:Vitellogenins; D004958:Estradiol; C025256:nonylphenol