Disrupting actions of bisphenol A and malachite green on growth hormone receptor gene expression and signal transduction in seabream.
Environmental estrogen could mimic natural estrogens thereby disrupting the endocrine systems of human and animals. The actions of such endocrine disruptors have been studied mainly on reproduction and development. However, estrogen could also affect the somatotropic axis via multiple targets such as growth hormone (GH). In the present study, two endocrine disruptors were chosen to investigate their effects on the expression level and signal transduction of growth hormone receptor (GHR) in fish. Using real-time PCR, it was found that exposure to both the estrogenic (bisphenol A) and anti-estrogenic (malachite green) compounds could attenuate the expression levels of GHR1 and GHR2 in black seabream (Acanthopagrus schlegeli) hepatocytes. The expression level of IGF-I, the downstream effector of GHR activation in the liver, was decreased by bisphenol A but not by malachite green. Luciferase reporter assay of the beta-casein promoter was used to monitor GHR signaling in transfected cells. In the fish liver cell line Hepa-T1, both GHR1 and GHR2 signaling were attenuated by bisphenol A and malachite green. This attenuation could only occur in the presence of estrogen receptor, indicating that these agents probably produce their actions via the estrogen receptor. Results of the present study demonstrated that estrogenic or anti-estrogenic compounds could down-regulate the somatotropic axis in fish by affecting both the gene expression and signaling of GHR. In view of the increasing prevalence of these compounds in the environment, the impact on fish growth and development both in the wild and in aquaculture would be considerable.
Jiao
Baowei
B
Department of Biochemistry and the Environmental Science Programme, The Chinese University of Hong Kong, Shatin, NT, Hong Kong, China.
Cheng
Christopher H K
CH
D000818:Animals; D001483:Base Sequence; D001559:Benzhydryl Compounds; D002478:Cells, Cultured; D017931:DNA Primers / Q000235:genetics; D052244:Endocrine Disruptors / Q000633:toxicity*; D004958:Estradiol / Q000494:pharmacology; D029941:Fish Proteins / Q000187:drug effects* / Q000235:genetics* / Q000378:metabolism; D015870:Gene Expression / Q000187:drug effects; D022781:Hepatocytes / Q000187:drug effects / Q000378:metabolism; D007334:Insulin-Like Growth Factor I / Q000187:drug effects / Q000235:genetics / Q000378:metabolism; D010636:Phenols / Q000633:toxicity*; D011986:Receptors, Somatotropin / Q000187:drug effects* / Q000235:genetics* / Q000378:metabolism; D012394:Rosaniline Dyes / Q000633:toxicity*; D021541:Sea Bream / Q000235:genetics* / Q000378:metabolism; D015398:Signal Transduction / Q000187:drug effects; D000098826:Bisphenol A Compounds
D001559:Benzhydryl Compounds; D017931:DNA Primers; D052244:Endocrine Disruptors; D004958:Estradiol; D029941:Fish Proteins; D007334:Insulin-Like Growth Factor I; D010636:Phenols; D011986:Receptors, Somatotropin; D012394:Rosaniline Dyes; C005095:malachite green; C006780:bisphenol A; D000098826:Bisphenol A Compounds
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