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  • Title: Hormonal effects on cell proliferation in rat prostate.
    Author: Bruchovsky N, Lesser B, Van Doorn E, Craven S.
    Journal: Vitam Horm; 1975; 33():61-102. PubMed ID: 180681.
    Abstract:
    Literature on the hormonal effects of cell proliferation in the rat prostate is reviewed. Prostatic growth is initiated when subnormal levels of glandular cells are present. During this process, DNA synthesis and cell proliferation are stimulated by androgens. During the phase of negative feedback that occurs when the number of cells returns to normal, DNA synthesis is decreased and cell proliferation is markedly reduced, though secretion continues to be stimulated by androgen. Autophagia begins after the withdrawal of androgens, and is characterized by extensive autolysis of cells and loss of functional per formance. Dihydrotestosterone (DHT) may be necessary for inducing mitotic activity during the phase of initiation, though DNA synthesis and cell division are not affected unless there are fewer than the normal number of cells. If the regenerative process is completed, the cells undergo 1.8 doublings with a doubling time of 40 hours and a division cycle time of 20 hours. In the negative feedback phase, the cell division potential is determined by the total number of prostate cells at the start of proliferation. Autophagia eliminates a large number of prostatic cells, with those remaining being available for androgen stimulation. It is possible that the growth response of the prostate may be influenced by enzymes that form or metabolize dihydrotestosterone and also by cytoplasmic receptors. Changes in the rates of DNA synthesis and cell proliferation do not coincide with the concentrations of cAMP, cytoplasmic receptor, and nuclear receptor durin g phases of prostatic involution. This implies that cAMP and androgen r eceptors are not directly responsible for regulating DNA synthesis and cell proliferation. It is suggested that the activity of homeostatic constraint mechanisms depends on the presence of initiator, nullifier, and autophage genes, and that the absence of lessening of growth-function genes is associated with the development of neoplasia.
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