CAJ | 학술논문

比较雌二醇（E2）、双酚A（BPA）、苯并[a]芘（B[a]P）和他莫昔芬（TAM）暴露对食蚊鱼（Gambusia affinis）卵黄蛋白原基因（VTGα）、雌激素受体基因（ERα）和细胞色素P4501A基因（CYP4501A）表达的影响。结果显示，低浓度E2单独暴露诱导VTGα和ERα表达量显著上调，但高浓度E2极显著抑制VTGα、ERα和CYP4501A表达。高浓度B[a]P明显抑制VTGα表达；B[a]P对ERa表达无明显抑制作用，但致CYP4501A表达量显著上升。 BPA显著上调VTGα和ERα的表达，但低浓度BPA致CYP4501A表达显著下降。 B[a]P＋高浓度E2联合暴露，致VTGα和ERα表达量显著提高，但B[a]P＋低浓度E2联合暴露抑制ERα的表达。 B[a]P＋E2不同浓度组均致CYP4501A表达水平呈极显著上升；B[ a] P＋E2＋TAM联合暴露均致VTGα、ERα和CYP4501A表达量显著或极显著增加。不同浓度组（B[a]P＋BPA）均致VTGα、ERα和CYP4510A表达量显著上调；B[a]P＋BPA＋TAM暴露，VTGα表达量呈极显著下降，相反，均致ERα和CYP4501A的表达量显著增加。单一毒物实验与联合毒物实验的比较表明，ERα和AhR介导的生理过程机制十分复杂，通过这两个途径对外来污染物的调控跟化合物的效应浓度有关，不是单独暴露效应的简单相加或相减。另外还进行E2／BPA＋B[ a] P＋TAM联合暴露实验，来研究TAM对ERα受体途径和AhR受体途径的影响，结果显示TAM对两个途径均有抑制作用。
비교자이순（E2）、쌍분A（BPA）、분병[a]비（B[a]P）화타막석분（TAM）폭로대식문어（Gambusia affinis）란황단백원기인（VTGα）、자격소수체기인（ERα）화세포색소P4501A기인（CYP4501A）표체적영향。결과현시，저농도E2단독폭로유도VTGα화ERα표체량현저상조，단고농도E2겁현저억제VTGα、ERα화CYP4501A표체。고농도B[a]P명현억제VTGα표체；B[a]P대ERa표체무명현억제작용，단치CYP4501A표체량현저상승。 BPA현저상조VTGα화ERα적표체，단저농도BPA치CYP4501A표체현저하강。 B[a]P＋고농도E2연합폭로，치VTGα화ERα표체량현저제고，단B[a]P＋저농도E2연합폭로억제ERα적표체。 B[a]P＋E2불동농도조균치CYP4501A표체수평정겁현저상승；B[ a] P＋E2＋TAM연합폭로균치VTGα、ERα화CYP4501A표체량현저혹겁현저증가。불동농도조（B[a]P＋BPA）균치VTGα、ERα화CYP4510A표체량현저상조；B[a]P＋BPA＋TAM폭로，VTGα표체량정겁현저하강，상반，균치ERα화CYP4501A적표체량현저증가。단일독물실험여연합독물실험적비교표명，ERα화AhR개도적생리과정궤제십분복잡，통과저량개도경대외래오염물적조공근화합물적효응농도유관，불시단독폭로효응적간단상가혹상감。령외환진행E2／BPA＋B[ a] P＋TAM연합폭로실험，래연구TAM대ERα수체도경화AhR수체도경적영향，결과현시TAM대량개도경균유억제작용。
This paper compares the VTGα, ERαand C YP4501A genes expression in liver tissue of immature male mosquitofish ( Gam-busia affinis) when combined with exposure to 17β-estradiol (E2), Bisphenol A (BPA), Benzo[a]Pyrene (B[a]P) and Tamoxifen ( TAM) , in order to research the co-effects and sole-effects of exogenous hormone.The results showed that, when single exposure to low concentration of E2,VTGαand ERαexpression was significantly up-regulated, but high concentration of E2 significantly inhibited VTGα, ERαand CYP4501A expression .High concentrations of B[a]P significantly inhibited VTGαexpression.B[a]P had no signifi-cant inhibitory effect on the expression of ERa, however, it caused a significant increase in the expression of CYP4501A.BPA signifi-cantly up-regulated VTGαand ERαexpression, however, lower concentrations of BPA decreased significantly CYP4501A expression. The joint exposure of B[a] P and high concentration E 2caused a significant increase of VTGαand ER αexpression levels, but the joint exposure of B[a]P and low concentration of E 2had no significant effect on ERαexpression.CYP4501A expression levels were signifi-cantly increased when exposed to different concentrations of (B[a]P+E2) groups;when exposed to (B[a]P+E2+TAM) groups, VTGα, ERαand CYP4501A expression was also significantly or very significantly increased.Different concentrations of ( B [ a] P+BPA) groups caused a significant up-regulating of VTGα, ERαand CYP45 01A expression levels.When exposed to (B [a] P +BPA+TAM) groups, VTGαexpression was significantly decreased; however,ER αandC YP4501A expression was significantly increased.The result indicated that the mechanism of AhR-ERαcross-talk pathway was complex, the regulation of this two pathway would be relevantto the effective concentration of chemicals.Comparing with the endocrine interferential effect induced by single chemical, the coeffectof the chemicals is related to exposure time and (or) the mixture concentration, not a simple addition of single one.We alsotreated the co-exposed of B[a]P and E2/BPA with TAM for the purpose of understanding the impact of Tamoxifen on AhR-ERa crosstalkpathway.Generally, the results suggested that TAM inhibit the expression of VTGα, ERαand CYP4 501A mRNA.