中文摘要：

为探讨邻苯二甲酸二G一乙基己谓自（DF_HP）和邻苯二甲酸单乙基己基酯（MEHP）长期暴露对海水生物的内分泌干扰效应及机制，将孵化后1周的海洋青鳉（Oryziay melastigma）分别暴露于DEHP（0．1 mg·L-1和05 mg·L-1）和MZrW（0．1 mg·L-1和05 mg·L-1）6个月。结果显示：DEHP显著增加了雌性和雄性海洋青鳉的肝指数，而MEHP只在高剂量时显著增加雄性青锵的肝指数。对于雌性青鳉，DE-HP暴露后肝脏雌激素相关基因ERα、ERβ、ERγ、VTG1、VTG2、ChgH和ChgL的表达水平显著上调，而对于雄性青鳉，DEHP暴露后，只有肝脏ERB的表达水平显著上调。相比之下，MEHP暴露对雌性和雄性青锵肝VTG和Chg基因表达无显著影响。DEHP激活了雌性和雄性青鳉的肝过氧化物增殖激活受体PPARα和PPARγ，而MEHP只在低剂量时上调了雄性青鳉PPARl的表达。在雌性和雄性青鳉体内，VTG和Chg的表达与ERα和ERγ的表达显著相关，并且ER与PPAR也显著相关。研究表明，DEHP长期暴露可通过激活肝性激素受体调控肝雌激素响应基因（VrG和chg）和过氧化物增殖激活受体（PPARα和PPARγ）的表达而对海洋青锵产生内分泌干扰效应，并且显示出性别特异性。MEHP对海洋青鳉的内分泌干扰效应弱于DEHP。

英文摘要：

To study the endocrine-disrupting effects and mechanisms of long-term eNposure to di（2-ethylhexyl）phthalate （DEHP） and mono （2-ethylhexyl） phthalate （MEHP） on marine aquatic organisms, Oryzias melastigma （oneweek post hatching） were eN0osed to DEHP （0.1 mg Ll and 05 mg·L-1） and MEHP （0.1 mg·L-1 and 05 mg·L-1） respec-tively for 6 months. The results showed that the hepatosomatic index （HSI） of female and male medaka increased af- ter exposure to DEHP. In contrast, the HSI of male fish increased significantly only after exposure to higher dose of MEHP （05 mg·L-1）. The mRNA levels of hepatic estrogen related genes including estrogen receptor （α, β, γ）, vitello- genin （VTG1, VTG2）, choriogenin （ChgL, ChgH） were significantly up-regulated in female medaka after exposure to DEHP. In male fish, only the expression of hepatic ERβ was significantly up-regulated after exposure to DEHP. In contrast, exposure to MEHP had no significant influence on the expression of VTG and Chg genes both for female and male. DEHP activated hepatic PPARα and PPARγ in both sexes, while only lower dose of MEHP （0.1 mg·L-1） augmented the expression of hepatic PPARγ in male. The expression of the VTG and Chg was significantly correla- ted to expression of the ERβ and ERγ in both female and male liver. Moreover, significant correlations were ob- served between the expression of ER and PPAR. Thus, it is proposed that endocrine-disrupting effects on marine medaka could be regulated through hepatic estrogenic responsive genes （VTG and Chg） and peroxisome prolifemtor- activated receptor （PPARα and PPARγ） after long-term exposure to DEHP, and the effect is sex-specific. MEHP showed weaker endocrine disrupting activity on marine medaka in comparison with that of DEHP.