Nicolas E, Goodyer I D, Taraschi T F
Department of Pathology, Anatomy and Cell Biology, Jefferson Medical College, 1020 Locust St., Philadelphia, PA 19107, USA.
Biochem J. 1997 Oct 15;327 ( Pt 2)(Pt 2):413-7. doi: 10.1042/bj3270413.
Inhibition of protein synthesis by cleavage of the N-glycosidic bond of a specific adenine of 28 S rRNA has been accepted as the mechanism by which plant ribosome-inactivating proteins (RIPs) cause cytotoxicity. The cytotoxic action of gelonin on Plasmodium falciparum malaria parasites appears to occur by a different mechanism. Parasite intoxication, which is manifested by mitochondrial dysfunction and lack of nucleic acid synthesis in the erythrocytic cycle following exposure to the toxin, is caused by the elimination of the parasite 6 kb extrachromosomal (mitochondrial) DNA. This is the first report which demonstrates that the DNA-damaging activities of RIPs observed in vitro can contribute to their cytotoxicity.
通过切割28 S rRNA特定腺嘌呤的N-糖苷键来抑制蛋白质合成，已被公认为是植物核糖体失活蛋白（RIPs）产生细胞毒性的机制。相思豆毒蛋白对恶性疟原虫的细胞毒性作用似乎是通过不同的机制发生的。寄生虫中毒表现为暴露于毒素后红细胞周期中的线粒体功能障碍和核酸合成缺乏，这是由寄生虫6 kb的染色体外（线粒体）DNA消除所致。这是第一份证明在体外观察到的RIPs的DNA损伤活性可导致其细胞毒性的报告。
