Olenyik Tamara, Gilroy Caslin, Ullman Buddy
Department of Biochemistry and Molecular Biology, Oregon Health & Science University, 3181 SW Sam Jackson Park Road, Portland, OR 97239-3098, USA.
Mol Biochem Parasitol. 2011 Apr;176(2):109-11. doi: 10.1016/j.molbiopara.2010.12.004. Epub 2010 Dec 21.
Administration of putrescine as a 1% solution in the drinking water ameliorated the profound loss of virulence exhibited by ornithine decarboxylase (ODC) deficient Leishmania donovani in mice. Furthermore, supplying α-difluoromethylornithine, an ODC inhibitor, at 2% in the drinking water reduced but did not eliminate infection with wild type L. donovani in the mouse model. Taken collectively, these findings: (1) demonstrate that oral putrescine can access the phagolysosome of macrophages in which the parasite resides in mice; (2) establish that the loss of virulence due to the Δodc lesion is a consequence of the inability of the mutant parasite to synthesize sufficient polyamines de novo; (3) imply that the L. donovani amastigote cannot access host polyamines in sufficient amounts for survival and growth; (4) and validate ODC as a drug target, although oral administration of DFMO is an unlikely therapeutic paradigm for visceral leishmaniasis.
在饮用水中以1%的溶液形式给予腐胺,可改善鸟氨酸脱羧酶(ODC)缺陷型杜氏利什曼原虫在小鼠体内所表现出的严重毒力丧失。此外,在饮用水中添加2%的ODC抑制剂α-二氟甲基鸟氨酸,可降低但不能消除小鼠模型中野生型杜氏利什曼原虫的感染。综合来看,这些发现:(1)表明口服腐胺可进入寄生虫在小鼠体内所寄生的巨噬细胞的吞噬溶酶体;(2)证实由于Δodc损伤导致的毒力丧失是突变寄生虫无法从头合成足够多胺的结果;(3)意味着杜氏利什曼原虫无鞭毛体无法获取足够量的宿主多胺以维持生存和生长;(4)并验证了ODC作为药物靶点,尽管口服DFMO不太可能成为内脏利什曼病的治疗模式。