Various pesticides known or suspected to interfere with steroid hormone function were screened toy effects in leydig cells on catalytic activity and mRNA expression of aromatase. Dichlorodiphenyltrichloroethane (DDT) is a widespread environmental pollutant. In this study, we investigated the effect of DDT on testosterone production through aromatase activity and its molecular mechanism in testicular leydig cell, R2C by using radioimmunoassay (RIA). As the results, the potent leydig: cell activator LH increased testosterone production compared to the control. DDT exposure significantly decreased testosterone production in R2C cell. In addition, DDT was found to increase aromatase gene expression and activity in R2C cell in a dose dependent manner. In order to assess whether the suppressive effects of DDT on LH-inducible testosterone (T) production might be influenced by the ER, ICI 182.780 was used, and it was found that these inhibitory effects of DDT were antagonized by ICI 182.780, implying that the estrogen receptor (ER) mediates the suppressive effects of DDT. Furthermore, the inducible effects of DDT on aromatase gene expression might be influenced by the ER, ICI 182.780 was used, and it was found that these enhancing effects of DDT were antagonized by ICI 182.780, implying that the ER mediates the inducible effects of DDT. Our results indicated that DDT inhibition of luteinizing hormone (LH) -inducible T production in R2C cell is mediated through aromatase. However, the precise mechanisms by which DDT enhance in R2C cell remains unknown. The current study suggests the possibility that DDT might act as a modulator aromatase gene transcription.