PubMedDate not supplied
The chlorinated pesticide, chlordecone, is widely recognized for its production of reproductive deficits. This reproductive sterility has been attributed to chlordecone's apparent "estrogenicity" and its ability to inhibit the release of luteinizing hormone (LH) from the anterior pituitary. However, it was recently noted that the pesticide could also reduce fertility when exposure was delayed until the day following ovulation. This led to the suggestion that chlordecone's actions on reproductive function continued into the postovulatory period. Results of the following studies substantiate this suggestion. Follicular development and ovulation were induced in immature female rats with a combined treatment of pregnant mare serum (PMS) and human chorionic gonadotropin (HCG). Chlordecone (25-75 mg/kg) administration at the time of PMS exposure did not inhibit the ovulatory response to HCG. Furthermore, when adult proestrous female rats were treated with chlordecone, normal numbers of ova were observed the following day. However, implantation sites were never observed in females that had been exposed to chlordecone. Moreover, offspring production was eliminated when mated females were exposed to doses of 50 or 75 mg/kg chlordecone on days 1, 2, or 3 following mating. In contrast, offspring production was normal when the exposure was delayed until the fourth day after mating. Since the vulnerable gestational period overlaps or precedes the time of implantation, these results suggest that ova viability and/or implantation is reduced by the chlordecone exposure.