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Biology of Reproduction 65, 1232-1237 (2001)
© 2001 Society for the Study of Reproduction, Inc.


Regular Article

Disparate Effects of Estradiol on Egg Transport and Oviductal Protein Synthesis in Mated and Cyclic Rats1

Pedro A. Orihuelaa, Mariana Ríosa, and Horacio B. Croxatto2,a

a Unidad de Reproducción y Desarrollo, Facultad de Ciencias Biológicas, Pontificia Universidad Católica de Chile, Santiago, Chile

ABSTRACT

{Previously, we found that the dose of estradiol (E2) required to accelerate egg transport increases 5- to 10-fold, in mated compared to cyclic rats. Here we examined protein synthesis in the oviduct of mated and cyclic rats following a single injection of E2 known to accelerate oviductal egg transport or after concomitant treatment with progesterone (P4) known to block this acceleration. On Day 1 of the cycle or pregnancy, E2, P4, or E2 + P4 were injected s.c., and 4 h later oviducts were removed and incubated for 8 h in medium with 35S-methionine. Tissue proteins were separated by SDS-PAGE, and protein bands were quantitated by fluorography and densitometry. In mated rats, E2 and P4 increased different protein bands and P4 did not affect the fluorographic pattern induced by E2. In contrast with mated rats, none of these treatments changed the fluorographic pattern of the oviductal proteins in cyclic rats. Estradiol-induced egg transport acceleration was then compared under conditions in which oviductal protein synthesis was suppressed. Mated and cyclic rats treated with equipotent doses of E2 for accelerating egg transport also received actinomycin D (Act D) locally. Estradiol-induced oviductal egg loss was partially blocked by Act D in mated but had no effect in cyclic rats. We conclude that the oviduct of mated and cyclic rats differs in that only the former responds with increased protein synthesis to a pulse of exogenous E2 and P4 and requires an intact protein synthesis machinery in order to accelerate egg transport in response to E2.

FOOTNOTES

First decision: 10 January 2001.

1 This work received financial support from grants from the Rockefeller Foundation (RF 94025 no. 15), World Health Organization (WHO CHI-LID-2), and FONDECYT 2990007 and 8980008, Cátedra Presidencial en Ciencias H Croxatto and MIFAB (Millennium Institute for Fundamental and Applied Biology).

2 Correspondence: H.B. Croxatto, Unidad de Reproducción y Desarrollo, Facultad de Ciencias Biológicas, Pontificia Universidad Católica de Chile, Casilla 114-D, Santiago, Chile. FAX: 56 2 222 5515;hbcroxat{at}genes.bio.puc.cl




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