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Search for other papers by M. R. BANERJEE in
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SUMMARY
The influence of oestradiol and progesterone on nucleic acids and protein synthesis during early development of 3- to 4-week-old C3H mouse mammary gland in vivo was studied. The hormones were administered daily by subcutaneous injections for 6–9 days. Uptake of tritium-labelled appropriate nucleoside and amino acid precursors, as determined by radio-chemical and autoradiographic methods, was used as a measure of cellular biosynthesis. Administration of the steroid hormones induces a pronounced increase of RNA, protein, and DNA synthesis in the mammary parenchyma of both intact and ovariectomized mice. Increased RNA and protein synthesis were detectable after two injections of the hormones, the maximal level was reached after the 6th injection. Hormone-induced DNA synthesis rose sharply reaching a peak after four treatments. The stimulatory effect of the steroids on DNA synthesis was more pronounced on the end-bud cells up to the 4th injection but in the duct cells [3H]thymidine uptake continued to rise progressively even after the 6th injection. Autoradiographs showed that the hormones also cause a twofold increase in the silver grain count per nucleus indicating an accelerated uptake rate of the DNA precursor. In end-bud cells mitotic activity, used as a measure of cellular proliferative activity, rose to a sharp peak after four injections of the hormones but in duct cells it continued to rise even after the 6th injection. The significance of these results with respect to further lobulo-alveolar development of the mammary parenchyma is discussed.
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Search for other papers by D. N. BANERJEE in
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SUMMARY
As measured by [3H]uridine incorporation in vivo, the low rate of RNA synthesis in the mammary gland of virgin C3H and BALB/c mice increased sixfold in the mammary tissue of 15-day pregnant mice. In the 5-day lactating gland, RNA synthesis was ten times higher than that in virgin mammary tissue. On the 10th day of lactation this increased RNA synthetic activity in the mammary gland was considerably reduced but was still twice that of the mammary tissue of virgin mice. Twenty-four hours after adrenalectomy, RNA synthesis in lactating glands was reduced by over 80%, whereas in the mammary gland before lactation, it was reduced by 20–30% only. A single i.p. injection of 250 μg of cortisol led to a threefold increase of RNA synthesis within 1 to 2 h in lactating glands of adrenalectomized mice; this was followed by a decline. Incorporation of [3H]leucine into trichloroacetic acid-insoluble material from lactating mammary tissue was used as a measure of'total protein' synthesis, and [3H]leucine radioactivity determined in Ca2+−rennin precipitate of 105000 g supernatant of lactating mammary tissue homogenate was used as a measure of casein synthesis. Adrenalectomy caused a 50% reduction of 'total protein' synthesis, whereas synthesis of 'casein-like' phosphoprotein virtually stopped after the operation. The injection of cortisol into adrenalectomized mice induced a selective increase of [3H]leucine incorporation into the casein of lactating glands. The results indicate that RNA synthesis in the mammary tissue is more dependent on adrenal hormones during the functional than the structural state of differentiation. The hormonal regulation of RNA synthesis and its role in milk protein synthesis in the mammary gland in vivo is discussed.
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A molecule very closely resembling human calcitonin immunologically and chromatographically was extracted from the nervous systems of several protochordates and a cyclostome, Myxine. The presence of human calcitonin-like molecules in the nervous systems of primitive chordates suggests that they have some function in the nervous system of these species and that the bone-regulating function of the calcitonins may have arisen much later in the vertebrates.
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Search for other papers by S J Rogers in
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Although previous studies have described the hypothalamo–pituitary–adrenal (HPA) response to the stress of acute myocardial infarction, it is not possible to study the hormone changes immediately after infarction in humans. Accordingly, we have examined the HPA response to microembolization of coronary arteries in 13 sheep compared with 5 sham control sheep. Plasma vasopressin (AVP; P<0·001), ACTH (P=0·005) and cortisol (P=0·005) were all increased 2 h (first sample time) after embolization. Plasma ACTH and cortisol levels returned to baseline levels by 6 h but plasma AVP levels did not return to baseline levels until more than 12 h after embolization. Plasma corticotrophin-releasing hormone (CRH) showed no significant change in response to embolization. In a subset of six animals which were sampled more frequently, the peak responses for plasma AVP, ACTH and cortisol occurred at 40 min after embolization. The maximum responses in any individual sheep observed at this time point were 744 pmol/l for AVP, 144 pmol/l for ACTH and 492 nmol/l for cortisol. CRH levels tended to increase across the first hour but these changes were not statistically significant. In conclusion, the stress hormone responses to microembolization of the coronary arteries have been defined in an ovine model of myocardial infarction. This model is suitable for studying the effects of novel treatments to reduce the stress of myocardial infarction.
Journal of Endocrinology (1997) 152, 489–493
