Oguro T, Numazawa S, Yoshida T, Kuroiwa Y
Department of Biochemical Toxicology, School of Pharmaceutical Sciences, Showa University, Tokyo, Japan.
Life Sci. 1989;45(11):963-70. doi: 10.1016/0024-3205(89)90149-5.
The administration of sulfobromophthalein (BSP, 0.5 mmol/kg, ip.) increased ornithine decarboxylase (ODC) and S-adenosylmethionine decarboxylase (SAMDC) activities to 30-fold and 5-fold, respectively, of the controls at 12 hr in the liver of rats. Parallel to the increase in ODC, there was an increase in hepatic putrescine content. However, spermine content tended to decrease. BSP increased ODC and SAMDC activities and putrescine content, but decreased spermine content, in a dose-dependent manner. Pretreatment of rats with actinomycin D and cycloheximide almost completely blocked the BSP-mediated increase of ODC and SAMDC activities. Pretreatment with glutathione (GSH) failed to inhibit BSP-mediated increase of ODC and SAMDC activities. In addition, the administration of BSP-GSH conjugate (0.5 mmol/kg, iv.) did not produce the increase of ODC and SAMDC activities. Pretreatment with phenobarbital and 3-methylcholanthrene did not inhibit BSP-mediated increase of ODC and SAMDC. The results indicate that BSP could cause changes in hepatic polyamine content due to the induction of ODC and SAMDC.
静脉注射磺溴酞钠(BSP,0.5 mmol/kg)使大鼠肝脏中的鸟氨酸脱羧酶(ODC)和S-腺苷甲硫氨酸脱羧酶(SAMDC)活性在12小时时分别增至对照组的30倍和5倍。与ODC活性增加同时,肝脏中腐胺含量增加。然而,精胺含量则有下降趋势。BSP以剂量依赖方式增加ODC和SAMDC活性及腐胺含量,但降低精胺含量。用放线菌素D和环己酰亚胺预处理大鼠几乎完全阻断了BSP介导的ODC和SAMDC活性增加。用谷胱甘肽(GSH)预处理未能抑制BSP介导的ODC和SAMDC活性增加。此外,静脉注射BSP-GSH缀合物(0.5 mmol/kg)未引起ODC和SAMDC活性增加。用苯巴比妥和3-甲基胆蒽预处理未抑制BSP介导的ODC和SAMDC增加。结果表明,BSP可通过诱导ODC和SAMDC而引起肝脏多胺含量变化。