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Estrogen-induced synthesis of riboflavin-binding protein in immature chicks. Kinetics and hormonal specificity
Insights
Estrogen rapidly increases riboflavin-binding protein in male chicks, with peak levels at 48 hours. This estrogenic response is blocked by antiestrogens, highlighting estrogen
Area of Science:
- Endocrinology
- Molecular Biology
- Reproductive Biology
Background:
- Riboflavin-binding protein (RBP) is a minor yolk constituent.
- Estrogen plays a role in regulating RBP levels.
Purpose of the Study:
- To investigate the kinetics of estrogen-induced RBP elevation in immature male chicks.
- To determine the effects of hormonal dose, secondary stimulation, and co-administered substances on RBP induction.
Main Methods:
- Radioimmunoassay (RIA) was used to measure plasma RBP concentration.
- 125I-labelled RBP was used to determine the circulating half-life.
- Estrogen, progesterone, and antiestrogens (cis- and trans-clomiphene citrates) were administered to chicks.
Main Results:
- Plasma RBP increased several-fold within 6 hours of estrogen injection, peaking at 48 hours.
- Secondary estrogen stimulation resulted in a two-fold amplification of the response.
- A 4-hour lag phase preceded RBP induction; dose-dependent magnitude but not timing was observed.
- The half-life of circulating RBP was approximately 10 hours.
- Progesterone did not affect RBP kinetics, while antiestrogens blocked estrogen-induced RBP elaboration.
Conclusions:
- Estrogen induces RBP production in male chicks with specific kinetics.
- The induction process involves a lag phase and is dose-dependent.
- Antiestrogens inhibit estrogen's effect on RBP, suggesting a receptor-mediated mechanism.
- Progesterone does not influence estrogen-induced RBP production.
Abstract:
The kinetics of estrogen-induced elevation in the plasma concentration of riboflavin-binding protein, a minor yolk constituent, was investigated in immature male chicks, using a specific and sensitive radioimmunoassay procedure. Following a single injection of the hormone, the plasma riboflavin-binding protein content was enhanced several-fold at 6 h, reaching peak levels around 48 h and declining thereafter. A two-fold amplification of the response was evident on secondary stimulation with the hormone. A 4-h lag phase prior to onset of induction was noticed during both primary and secondary stimulations with the steroid hormone. The magnitude of the response was dependent on the hormonal dose whereas the initial lag phase and the time of peak riboflavin-binding protein accumulation were unaltered within the range of hormonal doses tested. The half-life of riboflavin-binding protein in the circulation was 10 h, as calculated from measurement of the rate of disappearance of exogenously administered 125I-labelled protein. Simultaneous administration of progesterone did not affect the kinetics of riboflavin-binding protein production. On the other hand, the antiestrogens, cis- and trans-clomiphene citrates, given 30 min prior to estrogen and cycloheximide, effectively counteracted the hormone-induced riboflavin-binding protein elaboration. Both progesterone and the antiestrogens per se were completely ineffective in substituting for estrogen in the inductive process.