Impaired ovulation by 2,3,7,8 tetrachlorodibenzo-p-dioxin (TCDD) in immature rats treated with equine chorionic gonadotropin

Citation
K. Ushinohama et al., Impaired ovulation by 2,3,7,8 tetrachlorodibenzo-p-dioxin (TCDD) in immature rats treated with equine chorionic gonadotropin, REPROD TOX, 15(3), 2001, pp. 275-280
Citations number
25
Categorie Soggetti
da verificare
Journal title
REPRODUCTIVE TOXICOLOGY
ISSN journal
08906238 → ACNP
Volume
15
Issue
3
Year of publication
2001
Pages
275 - 280
Database
ISI
SICI code
0890-6238(200105/06)15:3<275:IOB2T(>2.0.ZU;2-E
Abstract
Several studies have established that 2,3,7,8 tetrachioro-p-dioxin (TCDD) b locks ovulation. The main purpose of this study was to determine if induced ovulation was delayed temporarily by TCDD. The ovulation model used was th at of the gonadotropin-primed intact or hypophysectomized rat. Immature int act female Sprague-Dawley rats (IIR) were given 32 mug TCDD/kg by gavage on day 24 of age. The next day equine chorionic gonadotropin (eCG) (5 IU) was injected sc to stimulate follicular development. The number of ova in the oviducts. the ovulation rate. and steroid concentrations were determined at 77, 96, 120, and 144 h after eCG. Immature female Sprague-Dawley rats (IHR ) were hypophysectomized on day 23 of age. On day 26, the IHR were given 20 mug TCDD/kg by gavage. The next day eCG (10 IU) was injected sc to stimula te follicle development and at 52 h after eCG, 10 IU human chorionic gonado tropin (hCG) was given to induce ovulation. The same parameters as in IIR w ere determined in IHR at 72, 96, and 120 h after eCG. TCDD decreased body a nd ovarian weight gains in both IIR and IHR. In IIR, TCDD delayed ovulation by 24 to 48 h reducing the number of ova shed as well as the number of ani mals ovulating at 72 and 96 h after eCG. In IHR, however, TCDD reduced only the number of ova shed but caused no delay in ovulation. The IIR treated w ith TCDD had low levels of progesterone (P4) at 72 and 96 h after eCG but h igh levels of estradiol (E2) at the same time points. This sustained high l evel of E2 production coincided with a transient decrease in serum concentr ations of androstenedione (Al). The alteration of steroid hormones by TCDD was restored to normal by 48 h after ovulation in IIR. Serum P4 concentrati on was not altered by TCDD in IHR at 72 h after eCG but was decreased there after. The delay in ovulation induced by TCDD in IIR indicates the disrupti on of the hypothalamus-pituitary-ovary axis during proestrus. The decrease in number of ova shed in IHR induced by exogenous gonadotropins indicates a n additional direct ovarian effect of TCDD in blocking ovulation. (C) 2001 Elsevier Science Inc. All rights reserved.