ANTAGONISTIC EFFECT OF ANDROGEN ON PROSTATIC CELL-DEATH
ANTAGONISTIC EFFECT OF ANDROGEN ON PROSTATIC CELL-DEATH
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DOI：
10.1002/pros.2990050510
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发表时间：
1984-01-01
期刊：
影响因子：
2.8
通讯作者：
ISAACS, JT
中科院分区：
文献类型：
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作者：
ISAACS, JT
雄激素除了具有刺激前列腺细胞增殖的明确激动能力外，还具有抑制前列腺细胞死亡的拮抗能力。这一说法是基于这样的观察：当血清睾酮水平足以长期维持腺体时，每天只有 2.1% 的前列腺细胞死亡；去势后3天，当血清睾酮水平<完整值的10%时，每天死亡的前列腺细胞总数百分比增加10倍，达到20.8%；如果通过外源睾酮治疗适当介导血清雄激素水平，那么去势后前列腺细胞的高死亡率可以得到抑制。拮抗性抑制前列腺细胞死亡所需的血清睾酮水平（即，1.4±0.1ng/ml）比拮抗性刺激前列腺细胞增殖所需的血清睾酮水平（3.3±0.4ng/ml）低>2倍。由于这种剂量差异，在实验上可以在去势大鼠中选择性地抑制前列腺细胞死亡而不同时刺激细胞增殖，并且仍然完全防止去势后前列腺的快速复旧。去势后前列腺的快速复旧主要是由于雄激素对前列腺细胞死亡的拮抗作用降低，而不是雄激素对前列腺细胞增殖的激动作用降低，并且这两种雄激素作用是前列腺中的不同过程。
Androgen, besides having the well-established agonistic ability to stimulate prostate cell proliferation, also has an antagonistic ability to inhibit prostatic cell death. This statement is based upon the observations that only 2.1% of the total prostatic cells die per day when serum testosterone level is sufficient for chronic maintenance of the gland; 3 days following castration, when serum testosterone level is < 10% of the intact value, the percentage of total prostatic cells now dying per day is increased 10-fold to a value of 20.8%; and this high rate of prostatic cell death can be inhibited following castration if serum androgen level is appropriately mediated by exogenous testosterone treatment. The serum testosterone level needed to antagonistically inhibitc prostatic cell death (i.e., 1.4 .+-. 0.1 ng/ml) is > 2-fold lower than that needed to antagonistically stimulate prostatic cell proliferation (3.3 .+-. 0.4 ng/ml). Due to this dose difference, it is experimentally possible in castrated rats to inhibit prostatic cell death selectively without simultaneously stimulating cell proliferation and still completely prevent the rapid involution of the prostate following castration. The rapid involution of the prostate following castration is predominantly due to a decreased antagonistic effect of androgen on prostatic cell death rather than to a decreased agonistic effect of androgen on prostatic cell proliferation and that these 2 androgenic effects are distinct processes in the prostate.