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 vol. 96 p. 1008 - 1014

0015-0282

OBJECTIVE: To investigate the underlying mechanisms implicated in the premature luteolysis induced by hyperthyroidism in pregnant rats. DESIGN: Experimental basic study. SETTING: Research institute. ANIMAL(S): Groups of 6-8 adult female Wistar rats were injected SC daily with T(4) (0.25 mg/kg) or vehicle, starting 8 days before mating, and killed by decapitation on days 19 (G19), 20 (G20), and 21 (G21) of pregnancy. INTERVENTION(S): Corpora lutea and truncal blood of control and hyperthyroid rats were obtained. MAIN OUTCOME MEASURE(S): Circulating and intraluteal hormones were determined by using RIA and luteal messenger RNA (mRNA) expression of enzymes and factors involved in P synthesis and metabolism by reverse transcriptase-polymerase chain reaction. 20α-Hydroxysteroid dehydrogenase (20αHSD) mRNA and protein expression was also determined by quantitative reverse transcriptase-polymerase chain reaction and Western blot. RESULT(S): Hyperthyroidism advanced luteolysis and 20αHSD expression induction by one day without changes in enzymes involved in P synthesis, decreased circulating E(2) and luteal estrogen receptor beta, and increased luteal prostaglandin F(2α) on G19 and G20 and prostaglandin E(2) on G19, while decreasing it on G20. Thus, decreased estrogenic influence and high prostaglandin F(2α)/prostaglandin E(2) ratio favors premature induction of 20αHSD on hyperthyroid rats. CONCLUSION: Hyperthyroidism affects luteolysis in pregnant rats through alterations in luteal prostaglandin balance and decreased luteotrophic factors favoring the luteolytic action of prostaglandin F(2α) that induces premature 20αHSD expression that in turn advances circulating P fall and delivery.