Lophirones B and C induce oxidative cellular death pathway in Acinetobacter baumannii by inhibiting DNA gyrase

被引:2
|
作者
Ajiboye, T. O. [1 ]
Aliyu, N. O. [1 ]
Ajala-Lawal, R. A. [1 ]
机构
[1] Nile Univ Nigeria, Coll Hlth Sci, Dept Med Biochem, Antioxidants Redox Biol & Toxicol Res Grp, Fct Abuja, Nigeria
关键词
Oxidative DNA damage; Lophirones B and C; Acinetobacter baumannii; Fenton chemistry; Hydroxyl radical; DNA gyrase A; CHALCONE DIMERS; OXYGEN; ANTIBIOTICS; STRESS; DAMAGE; REDOX; IRON; INVOLVEMENT; SUPEROXIDE;
D O I
10.1016/j.micpath.2019.03.011
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
We evaluated the inactivation of DNA gyrase on the oxidative stress response and sensitivity of A. baumannii to lophirones B and C. The sensitivity of parental and the mutant strains of A. baumannii to lophirones B and C was determined using minimum inhibitory concentration (MIC) and time-kill sensitivity. Inactivation of sodB, katG, recA enhanced the sensitivity of A. baumannii to lophirones B and C. Furthermore, this inactivation increased the accumulation of superoxide anion radical and hydrogen peroxide in lophirones B and C-treated A. baumannii, which was reversed in the presence of thiourea. Inactivation of gyrA stalled lophirones B and C-mediated ROS accumulation in A. baumannii. In addition, lophirones B and C raised the Fe2+ contents of A. baumannii. Dipyridyl (Fe chelator) reversed the sensitivity of A. baumannii to lophirones B and C. Lophirones significantly lowered the NAD + /NADH ratio of A. baumannii. The results of this study revealed that the impact of DNA gyrase in lophirones B and C-mediated ROS accumulation, Fe2+ release and cell death.
引用
收藏
页码:226 / 231
页数:6
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