Estensen R D, Baserga R
J Cell Biol. 1966 Jul;30(1):13-22. doi: 10.1083/jcb.30.1.13.
Chemical and radioautographic analysis of the small intestine of mice injected intraperitoneally with puromycin revealed an immediate decrease of precursor incorporation into DNA and protein and a delayed decrease of precursor incorporation into RNA. In addition to this decrease of precursor incorporation, damage to the crypt cells, but not to the cells of the villus of the small intestine, was observed. Further examination of other dividing cells (spleen) and nondividing cells (liver and heart) of these mice showed again that only cells of actively dividing tissues were damaged. The metabolic inhibitors actinomycin D, cytosine arabinoside, actidione, and puromycin aminonucleoside were used in an attempt to clarify the mechanism of cell damage by puromycin. The results showed that there was no clear correlation between cell necrosis and the pattern of inhibition of synthesis of DNA, RNA, or protein.
对经腹腔注射嘌呤霉素的小鼠小肠进行化学和放射自显影分析显示，前体掺入DNA和蛋白质的量立即减少，而前体掺入RNA的量则延迟减少。除了前体掺入减少外，还观察到小肠隐窝细胞受损，但绒毛细胞未受损。对这些小鼠的其他分裂细胞（脾脏）和非分裂细胞（肝脏和心脏）进行进一步检查再次表明，只有活跃分裂组织的细胞受到了损伤。使用代谢抑制剂放线菌素D、阿糖胞苷、放线菌酮和嘌呤霉素氨基核苷来试图阐明嘌呤霉素导致细胞损伤的机制。结果表明，细胞坏死与DNA、RNA或蛋白质合成抑制模式之间没有明显的相关性。
