STUDIES ON GLUTATHIONE METABOLISM IN VENTRAL PROSTATE AND CHEMICALLY-INDUCED PROSTATIC-CARCINOMA IN RATS
STUDIES ON GLUTATHIONE METABOLISM IN VENTRAL PROSTATE AND CHEMICALLY-INDUCED PROSTATIC-CARCINOMA IN RATS
复制标题
DOI：
10.1007/bf01122456
复制
发表时间：
1983-01-01
影响因子：
4
通讯作者：
VIJAYVARGIYA, R
中科院分区：
文献类型：
--
作者：
SINGHAL, RL;VIJAYVARGIYA, R
用化学诱导法诱发11095例大鼠前列腺癌模型，测定其腹侧前列腺癌组织中谷胱甘肽含量和谷胱甘肽还原酶活性。去势后，前列腺中还原型谷胱甘肽(GSH)和氧化还原型谷胱甘肽(GSSG)和谷胱甘肽还原酶活性显著降低。去势动物每日补充睾酮(50 mg/kg)，连续7天，可使还原型谷胱甘肽水平和谷胱甘肽还原酶活性接近正常水平。将鳞状细胞癌植入去势后的完整动物体内。在植入后21天，正常大鼠的肿瘤生长导致腹侧前列腺重量减少了近30%，尽管谷胱甘肽水平没有受到影响。与正常组织相比，在肿瘤中检测到的谷胱甘肽还原酶的活性要高得多。肿瘤的GSH/GSSG比值也显著升高。无论是在正常动物体内还是在去势的动物体内，肿瘤的生长速度都没有明显差异。在从两组动物获得的肿瘤中，还原和氧化的谷胱甘肽和谷胱甘肽还原酶活性的水平似乎也是相同的。去势荷瘤动物连续11天每日给予睾酮(50 mg/kg)或β-雌二醇(2 mg/kg)，并不改变谷胱甘肽水平和谷胱甘肽还原酶活性。与正常受试者相比，携带肿瘤的大鼠血液中还原型谷胱甘肽水平显著升高。雄激素耗竭和替代治疗影响大鼠前列腺腹侧谷胱甘肽的代谢。在观察到的雄激素效应方面，前列腺癌似乎与正常组织不同。与腹侧前列腺癌相比，肿瘤组织中谷胱甘肽还原酶活性较高，还原型谷胱甘肽含量较低，因此两种组织中谷胱甘肽的代谢不同。β-雌二醇是一种抗前列腺癌药物，它的治疗似乎不会影响前列腺癌的生长或谷胱甘肽代谢。血中谷胱甘肽水平的变化可作为肿瘤组织快速生长的指标。
Glutathione content and the activity of glutathione reductase were examined in ventral prostate and chemically induced 11095 squamous cell prostatic carcinoma in rats. Castration produced a significant reduction in the levels of reduced (GSH) and oxidized (GSSG) glutathione and glutathione reductase activity in the prostate. Replacement of testosterone (50 mg/kg) daily for 7 days to castrated animals elevated the reduced glutathione level and the activity of glutathione reductase almost to normal limits. Squamous cell carcinoma was implanted in castrated and intact animals. Tumor growth in normal rats produced a decrease of almost 30% in the weight of the ventral prostate at 21 days post-implantation, although the glutathione levels remained unaffected. Much greater activity of glutathione reductase was detected in the tumor in comparison to the values noted for the normal tissue. The tumor also showed significantly higher values for the GSH/GSSG ratio. No apparent difference could be found in the rate of the growth of tumors whether implanted in normal or castrated animals. The levels of reduced and oxidized glutathione and glutathione reductase activity also seemed identical in tumors obtained from both groups of animals. Administration of testosterone (50 mg/kg) or .beta.-estradiol (2 mg/kg) daily for 11 days to tumor-bearing castrated animals did not alter the levels of glutathione and glutathione reductase activity. A significantly higher level of blood reduced glutathione was found in tumor-bearing rats in comparison to that seen for the normal subjects. Androgen depletion and replacement therapy influence the metabolism of glutathione in rat ventral prostate. Squamous cell carcinoma of the prostate appears to differ from the normal tissue with respect to the observed androgen effects. There is dissimilarity in the metabolism of glutathione in the 2 tissues since greater activity of glutathione reductase and lower values of reduced glutathione were seen in the tumor compared to those of the ventral prostate. Treatment with .beta.-estradiol, an antiprostatic agent, does not seem to influence the growth or glutathione metabolism of squamous cell carcinoma of the prostate. The observed changes in blood glutathione levels might be useful as an index of rapid growth of the neoplastic tissue.