免賴得和貝芬替均為廣泛使用之系統性殺菌劑，先前我們研究已顯示免賴得與貝芬替在生殖與發育毒性 試驗中可誘發大鼠荷爾蒙干擾作用及雄性素受體基因表現。因此本試驗目的在進一步利用雌大鼠子宮激性與 雄大鼠副性腺激性測試免賴得與貝芬替對大鼠之荷爾蒙干擾作用。在子宮激性試驗結果顯示單處理免賴得與 貝芬替除最高劑量800 mg/kg/day外，相較於對照組，未顯著改變子宮與陰道相對重。共處理雌素二醇與200 mg/kg/day免賴得或雌素二醇與200、800 mg/kg/day貝芬替較單處理雌素二醇顯著增加子宮重量。共處理雌素二 醇與免賴得或貝芬替所增加子宮重量可能是透過雄性素受體傳遞的。單處理氟他胺(Flutamide)也未改變子宮 相對重。共處理雌素二醇與Flutamide相較於單處理雌素二醇未影響子宮相對重。在副性腺激性試驗，單處理50、100 mg/kg/day免賴得顯著增加前列腺與貯精囊重，但貝芬替與Flutamide則否。共處理睪固酮丙酸鹽與50、 100 mg/kg/day貝芬替相較於單處理睪固酮丙酸鹽顯著增加前列腺與貯精囊相對重，但免賴得則否。共處理睪 固酮丙酸鹽與Flutamide 50、100 mg/kg/day相較於單處理睪固酮丙酸鹽則顯著降低上述副性腺相對重。根據本 實驗室先前報告文獻顯示，投予懷孕母鼠貝芬替，回復Flutamide所降低雄仔鼠前列腺與貯精囊重及誘發睪丸 副睪及副性腺雄性素受體mRNA與蛋白表現，因此推論免賴得與貝芬替增加前列腺與貯精囊重經由雄性素受 體傳導。另根據Wolf等(2002)報告顯示，子宮激性所增加之子宮液可能也是透過雄性素激性所致。綜合上述結 果，免賴得與貝芬替可能透過雄性素受體顯著誘發年輕成熟大鼠與雄性素作用而增加貯精囊與前列腺重及子 宮液滯留，但確實作用機制仍需進一步探討。

Both benomyl and carbendazim are widely used systemic fungicides. It has been shown that benomyl and carbendazim induce endocrine-disrupting activity, resulting in reproductive and developmental toxicity, as well as androgen receptor (AR) gene expression in rats. The aim of this study was to link AR induction by benomyl and carbendazim, observed in our previous reports, with the results of Hershberger and uterotrophic assays. In an uterotrophic assay, neither benomyl nor carbendazim, except at 800 mg/kg/day, affected weight of uterus and vagina when compared to the ovariectomized control rats. Co-treatment with 17β-estradiol (E2) and 200 mg/kg/day benomyl or co-treatment with E2 and 200, 800 mg/kg/day carbendazim significantly increased uterine weight when compared to treatment with E2 alone in an uterotrophic assay. This uterotrophic activity might be mediated through AR. Treatment with flutamide alone or in combination with E2 had no effect on uterine weight. In the Hershberger assay, treatment with 50 and 100 mg/kg/day benomyl increased weight of ventral prostate plus seminal vesicles. Carbendazim or flutamide alone exhibited no effect on reproductive accessory gland weight. Co-treatment with testosterone propionate (TP) and 50 or 100 mg/kg/ day carbendazim, but not benomyl, significantly increased the weight of ventral prostate plus seminal vesicles. Co-treatment with TP and 50 or 100 mg/kg/day flutamide significantly decreased these reproductive accessory gland weights when compared with TP alone. Based on our previous report, carbendazim increases mRNA and protein expression of AR in testis, epididymis and prostate and antagonizes the reduced tissue weights of seminal vesicle and prostate of male offsprings induced by in utero exposure to flutamide in rats. This infers that benomyl and carbendazim increase the weight of ventral prostate plus seminal vesicles through induction of AR expression. Moreover, according to a previous report, TP, an AR agonist, induces fluid retention in uterus by exhibiting androgenic activity, similar to that of benomyl and carbendazim, in an uterotrophic assay. Based on these results, benomyl and carbendazim exhibit an androgenic effect, leading to increased weight of ventral prostate and seminal vesicles and uterine fluid retention in young adult rats. The exact mechanisms require further investigation.