RESUMEN

Avidin induction in chick tissues in vivo and in vitro was studied by a phosphodiesterase inhibitor, theophylline, and compared to progesterone-dependent induction. Theophylline (100 mg/kg, ip) caused a significant increase in avidin content only in the oviduct of diethylstilbestrol-treated chicks, but not in the lung, muscle, intestine, plasma, or in the bursa of Fabricius. Diethylstilbestrol priming was necessary for oviductal avidin induction in vivo by theophylline. In the oviduct culture, theophylline at a concentration between 100 and 500 micrograms/ml caused a dose-dependent increase in avidin production. Effects of theophylline and progesterone on avidin synthesis in oviduct culture were synergistic. Avidin production was dependent on protein and RNA synthesis, since induction was inhibited by cycloheximide and actinomycin D. Avidin induction by theophylline resembled progesterone-dependent induction, beginning 9 h after the injection in vivo and 12 h after administration of these drugs in vitro. Avidin induced by theophylline showed heat-induced biotin exchange identical to that of progesterone-induced avidin, indicating close similarity of these proteins. The results suggest that theophylline can mimic the action of progesterone on avidin production, and that cyclic nucleotides may have a role in the regulation of avidin synthesis.

Asunto(s)

RESUMEN

Regulation of avidin accumulation by prostaglandins (PGs) and their inhibitors was studied in chick oviduct organ culture. Avidin was induced neither by progesterone nor PGF2 alpha in the oviduct of immature chicks. By progesterone and PGs, a high avidin synthesis was induced when the chicks received diethylstilbestrol (DES) for 7 days. Enhanced avidin production was observed by PGF2 alpha, PGE1 and PGE2, whereas PGA2 and PGB2 had a slight inhibitory effect and PGA1 and PGB1 had no effect on avidin production. PGF2 alpha was most effective at a concentration of 10-20 micrograms/ml. The effects of progesterone and PGF2 alpha were not additive. Mefenamic acid, at concentrations of 40 and 60 micrograms/ml, inhibited 50 and 85%, respectively, of the avidin synthesis induced by progesterone, whereas the inhibition of the total protein synthesis was only 20%, and this only by the higher concentration of the drug. Tolfenamic and meclofenamic acid were also inhibitory in the case of progestin-induced avidin synthesis. These studies indicate that the PGs (F2 alpha, E1 and E2) might be involved in the avidin induction in the chick differentiated oviduct. The specific inhibition of the progesterone-dependent avidin synthesis by the PG inhibitors suggests that PGs may be connected with the progesterone action in the oviduct. We propose that the avidin synthesis by the chick oviduct might be considered as a model system for studying PG effects on the synthesis of a specific protein.

Asunto(s)

RESUMEN

The growth and differentiation of chick oviducts were caused by daily diethylstilboestrol (DES) or oestradiol-17 beta (E2) injections, and the effects of these oestrogens on the progesterone-induced production of a biotin-binding egg-white protein (avidin) were studied. In the DES primed oviducts, but not in the E2 primed ones, both DES and E2 administered with progesterone potentiated avidin production 2 to 3-fold, even after 10-day oestrogen withdrawal. The results suggest that DES and E2 prime the avian reproductive target tissue differently.

Asunto(s)

RESUMEN

The effects of diethylstilboestrol (DES) and oestradiol-17 beta on the production of a progesterone-induced protein (avidin) in the chick oviduct were studied. Chicks were pretreated with DES or oestradiol-17 beta daily for 3-28 days and progesterone (10 or 20 mg/kg) was administered 24 h after the last oestrogen injection. Diethylstilboestrol (2-20 mg/kg) administered with progesterone to chicks pretreated with DES increased avidin production after 16 h compared with that induced by progesterone alone. The potentiation of avidin production appeared even when DES was administered between 6 h before and 13 h after progesterone injection. The length of DES pretreatment did not affect the potentiation. The amount of avidin induced by progesterone in the chicks pretreated with oestradiol-17 beta was similar to that in the chicks pretreated with DES. Oestradiol-17 beta (2-20 mg/kg) administered with progesterone, however, did not affect avidin production. The results suggest that DES may have some non-oestrogenic effects on the production of progesterone-induced proteins.

Asunto(s)

Asunto(s)

RESUMEN

Biotin-binding and immunological methods were employed to demonstrate the similarity of oviduct and non-oviduct avidin in the chicken. Oviduct avidin was induced after oestrogen pretreatment by progesterone and non-oviduct avidin by intestinal tissue injury or by intraperitoneal actinomycin D administration. Avidin in the intestine, lung, bursa of Fabricius, plasma, pectoral muscle and liver after injury had biotin-binding activity similar to that of progesterone-induced oviduct avidin: (1) a temperature of 79-83 degree C was required for 50% of the maximum [14C]biotin uptake, (2) maximal exchange occurred only at 90 or 100 degree C and (3) denaturation of protein, i.e., loss of biotin-binding activity, was not yet observed at 100 degree C. Avidin in the intestine, lung, bursa of Fabricius, plasma and pectoral muscle also showed an identical cross-reaction with oviduct avidin. Furthermore, the increase in avidin-like biotin binding in the oviduct and most non-oviduct tissues was significantly correlated with the increase in avidin-like antigen in the tissue. This indicates that avidin induced in chicken non-oviduct tissues by injury or inflammation caused by actinomycin D administration is similar to progesterone-dependent oviduct avidin.

Asunto(s)

Asunto(s)