期刊
INTERNATIONAL JOURNAL OF BIOLOGICAL MACROMOLECULES
卷 95, 期 -, 页码 145-152出版社
ELSEVIER
DOI: 10.1016/j.ijbiomac.2016.11.038
关键词
E. coli ATP synthase; F-1 F-0 -ATP synthase; ATP synthesis; Safranal; Thymol; Cuminol; Carvacrol; Damascenone
资金
- National Institutes of Health [GM085771]
- A.T. Still University-Kirksville College of Osteopathic Medicine Biomedical Science Graduate Program [850-619]
- Kirksville College of Osteopathic Medicine
Safranal, a dominant component of saffron, is known to have antitumor, cytotoxic, and antibacterial properties. In this study, we examined safranal and its structural analogs thymol, carvacrol, damascenone, cuminol, 2,6,6-trimethy1-2-cyclohexene-1,4-dione (TMCHD), 4-isopropylbenzyl bromide (IPBB), and 4-tert-butylphenol (TBP) induced inhibition of Escherichia coli membrane bound F1F0 ATP synthase. Safranal and its analogs inhibited wild-type enzyme to variable degrees. While safranal caused 100% inhibition of wild-type F1F0 ATP synthase, only about 50% inhibition occurred for alpha R283D mutant ATP synthase. Moreover, safranal, thymol, carvacrol, damascenone, cuminol, TMCHD, IPBB, and TBP all fully abrogated the growth of wild-type E. coli cells and had partial or no effect on the growth of null and mutant E. coli strains. Therefore, the antimicrobial properties of safranal, thymol, carvacrol, damascenone, cuminol, TMCHD, IPBB, and TBP can be linked to their binding and inhibition of ATP synthase. Total loss of growth in wild-type and partial or no growth loss in null or mutant E. coli strains demonstrates that ATP synthase is a molecular target for safranal and its structural analogs. Partial inhibition of the alpha Arg-283 mutant enzyme establishes that alpha Arg-283 residue is required in the polyphenol binding pocket of ATP synthase for the binding of safranal. Furthermore, partial growth loss for the null and mutant strains in the presence of inhibitors also suggests the role of other targets and residues in the process of inhibition. (C) 2016 Elsevier B.V. All rights reserved.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据