HYPERTHYROIDISM ADVANCES LUTEOLYSIS IN THE PREGNANT RAT THROUGH CHANGES IN PROSTAGLANDIN BALANCE.

NAVAS PB; MOTTA, AB; HAPON MB; JAHN GA

FERTILITY AND STERILITY

ELSEVIER SCIENCE INC

Año: 2011

0015-0282

Objective: Investigate the underlying mechanisms implicated in the premature luteolysis induced by hyperthyroidism in pregnant rats. Design: Experimental basic study Setting: Research Institute Animals: Groups of 6- 8 adult female Wistar rats were injected s.c. daily with T4 (0.25 mg/kg) or vehicle, starting 8 days before mating and sacrificed by decapitation on days 19 (G19), 20 (G20) and 21 (G21) of pregnancy. Intervention(s): Corpora lutea (CL) and troncal blood of control and hyperthyroid rats were obtained. Main Outcome Measures: Circulating and intraluteal hormones were determined by radioinmunoassay and luteal messenger RNA (mRNA) expression of enzymes and factors involved in progesterone (P4) synthesis and metabolism by RT-PCR. 20α hydroxysteroid dehydrogenase (20αHSD) mRNA and protein expression was also determined by quantitative RT-PCR and Western blot. Results: Hyperthyroidism advanced luteolysis and 20αHSD expression induction by one day without changes in enzymes involved in P4 synthesis, decreased circulating E2 and luteal ERβ, and increased luteal prostaglandin F2α (PGF2α) on G19 and G20 and PGE2 on G19, while decreasing it on G20. Thus, decreased estrogenic influence and high PGF2α/PGE2 ratio favours premature induction of 20αHSD on hyperthyroid rats. Conclusion: Hyperthyroidism affects luteolysis in pregnant rats through alterations in luteal prostaglandin balance and decreased luteotrophic factors favouring the luteolytic action of PGF2α that induces premature 20αHSD expression that in turn advances circulating P4 fall and delivery.