A number of studies have reported that reproductive and developmental disorders are produced by prenatal or postnatal exposure to dioxins such as 2,3,7,8-tertachlorodibenzo-p-dioxin (TCDD). These effects would be more serious compared with other toxicities with dioxins, because those injuries appear at much lesser doses than those needed for acute toxicity. Although the mechanisms regulating reproductive and developmental disorders are still unclear, we have recently reported that maternal exposure to TCDD causes the suppression of fetal testicular steroidogenic enzymes in rats. In the present study, we examined whether the same occurs in mice, using C57BL/6J and DBA/2N strains. The result showed that TCDD does not show any effect on the expression of steroidogenic acute regulatory protein mRNA in both strains. To the best of our knowledge, abnormal sexual behavior by fetal exposure to TCDD has never been reported in mice. Therefore, our result supports a possibility that abnormal sex behavior by exposure to TCDD at the fetal stages occurs in rats but not in mice. In addition, the data obtained suggest that the suppression of fetal testicular steroidogenic enzymes is, at least, one of the key mechanisms for impaired sex behavior induced by dioxin.
|Number of pages||5|
|Journal||Fukuoka igaku zasshi = Hukuoka acta medica|
|Publication status||Published - Jan 1 2007|
All Science Journal Classification (ASJC) codes