title: Influence of the formamidine pesticide chlordimeform on ovulation in the female hamster: dissociable shifts in the luteinizing hormone surge and oocyte release.
abstract: The formamidine pesticide chlordimeform (CDF) has been found to interfere with the hormonal control of ovulation in the rat by a presumptive disruption in the catecholaminergic regulation of the midcycle surge of luteinizing hormone (LH). While the brain hypothalamic mechanisms underlying generation of the hamster surge have not been as well-defined, there is evidence for an adrenergic component. The present experiments were designed to investigate the effects of CDF on ovulation in the golden hamster and whether any observed alterations are associated with differences in the appearance of the surge. Intraperitoneal CDF injections (0, 75, 150, or 200 mg/kg) at 1400 hr on proestrus caused a dose-related reduction in oocytes retrieved at 0700 hr on the day of estrus. Additional experiments demonstrated that this effect was due to a delay in ovulation and not a decrease in the complement of oocytes released. Doses of 150 or 200 mg/kg at 1100 hr or 200 mg/kg at 1600 hr were without a comparable ovulatory effect. Characterization of the LH surge indicated that there was a dose-related delay, but that this effect was not sufficient to account for the delay in ovulation. Animals dosed at 1100 hr (150 or 200 mg/kg) exhibited shifts in the surge identical to those animals injected at 1400 hr, but did not show any such detectable effects on the time of oocyte release. CDF administered at 1100 or 1400 hr also caused alterations in serum estradiol and progesterone, even at a relatively low dose of 37.5 mg/kg. The results indicate that CDF given at a time just prior to the preovulatory rise in LH is able to impede ovulation in the hamster by possibly influencing some ovulatory event(s) triggered by the surge. Also, the ability of CDF to alter the timing of LH release is consistent with catecholaminergic participation in the generation of the gonadotropin signal stimulating the final events leading to ovulation. Under the present conditions, this perturbation can be characterized as a delay in the LH trigger, rather than a blockade.
authors.affiliation: Reproductive Toxicology Branch, U.S. Environmental Protection Agency, Research Triangle Park, North Carolina 27711.
authors.forename: J M
authors.initials: JM
authors.lastname: Goldman
authors.forename: T E
authors.initials: TE
authors.lastname: Stoker
authors.forename: S D
authors.initials: SD
authors.lastname: Perreault
authors.forename: R L
authors.initials: RL
authors.lastname: Cooper
authors.forename: M A
authors.initials: MA
authors.lastname: Crider
mesh_terms: D000818:Animals; D002742:Chlorphenamidine / Q000008:administration & dosage / Q000494:pharmacology*; D006224:Cricetinae; D004305:Dose-Response Relationship, Drug; D004958:Estradiol / Q000097:blood; D005260:Female; D005640:Follicle Stimulating Hormone / Q000097:blood; D007274:Injections, Intraperitoneal; D007986:Luteinizing Hormone / Q000187:drug effects* / Q000378:metabolism; D009865:Oocytes / Q000187:drug effects*; D010060:Ovulation / Q000187:drug effects* / Q000378:metabolism; D011359:Proestrus / Q000187:drug effects / Q000502:physiology; D011374:Progesterone / Q000097:blood
chemical_list: D011374:Progesterone; D004958:Estradiol; D007986:Luteinizing Hormone; D005640:Follicle Stimulating Hormone; D002742:Chlorphenamidine