Laitinen S I, Pajunen A E
Biochem Biophys Res Commun. 1983 Apr 29;112(2):770-7. doi: 10.1016/0006-291x(83)91528-0.
The effect of inhibition of polyamine synthesis on castrated male mouse kidney beta-glucuronidase induction and secretion by testosterone was studied. Inhibition of the activities of polyamine synthesis key-enzymes, L-ornithine and S-adenosyl-L-methionine decarboxylases, was performed with the combined treatment of 2-difluoromethylornithine and methylglyoxal' bis(guanylhydrazone). Blockage of polyamine synthesis did not affect testosterone-induced increase in renal beta-glucuronidase but blocked its secretion into the urine. After withdrawal of inhibitor-treatment beta-glucuronidase secretion normalized, and repeated testosterone administration produced undisturbed beta-glucuronidase secretion peak in urine suggesting that blockage of beta-glucuronidase secretion was not due to the tissue damage produced by inhibitors. These results indicate that the stimulation of renal polyamine synthesis by testosterone is not necessary for the induction of beta-glucuronidase but is required for the urinary secretion of this protein.
研究了多胺合成抑制对去势雄性小鼠肾脏β-葡萄糖醛酸酶诱导及睾酮分泌的影响。采用2-二氟甲基鸟氨酸和甲基乙二醛双（胍腙）联合处理抑制多胺合成关键酶L-鸟氨酸和S-腺苷-L-蛋氨酸脱羧酶的活性。多胺合成的阻断不影响睾酮诱导的肾脏β-葡萄糖醛酸酶增加，但阻断了其向尿液中的分泌。抑制剂处理撤除后，β-葡萄糖醛酸酶分泌恢复正常，重复给予睾酮可使尿液中β-葡萄糖醛酸酶分泌峰不受干扰，这表明β-葡萄糖醛酸酶分泌的阻断并非由于抑制剂产生的组织损伤所致。这些结果表明，睾酮刺激肾脏多胺合成对于β-葡萄糖醛酸酶的诱导并非必要，但对于该蛋白的尿液分泌是必需的。
