（Rv3340）衍生的硫化氢赋予细菌应激生存能力。

(Rv3340) derived hydrogen sulphide conferring bacteria stress survival.

机构信息

a Institute of Modern Biopharmaceuticals, State Key Laboratory Breeding Base of Eco-Environment and Bio-Resource of the Three Gorges Area, Ministry of Education, School of Life Sciences, Southwest University , Chongqing , China.

b Department of Clinical Microbiology, College of Medical Laboratory Sciences, Omdurman, Islamic University , Omdurman , Sudan.

出版信息

J Drug Target. 2019 Nov;27(9):1004-1016. doi: 10.1080/1061186X.2019.1579820. Epub 2019 Mar 21.

DOI:10.1080/1061186X.2019.1579820

PMID:30730218

Abstract

Tuberculosis, especially multidrug resistant cases, remains an enormous public health threat. (Rv3340) an enzyme involved in methionine biosynthesis was identified and characterised for antimicrobial susceptibility. We reported that the overexpression of Rv3340 in (Ms_Rv3340) produces hydrogen sulphide (HS) for its energy in harsh conditions. The produced HS sustained Ms_Rv3340 against streptomycin, whereas the chemical inhibition of HS caused streptomycin lethality to Ms_Rv3340. Further analysis showed that cysteine-HO treatment of Ms-Rv3340 initiated DNA damage via Fenton reaction. Ms_Rv3340 downregulated the expression levels of three streptomycin responsive genes. To our knowledge, no study has been previously reported that (Rv3340) can generates HS modulating resistant to streptomycin which provides a greater perception toward the treatment and control of tuberculosis.

摘要

结核病，尤其是耐多药病例，仍然是一个巨大的公共卫生威胁。（Rv3340）一种参与蛋氨酸生物合成的酶被鉴定并进行了抗菌药物敏感性特征分析。我们报道，（Ms_Rv3340）中 Rv3340 的过表达在恶劣条件下产生硫化氢（HS）作为其能量来源。产生的 HS 使 Ms_Rv3340 对链霉素具有耐受性，而 HS 的化学抑制导致 Ms_Rv3340 对链霉素的致死性。进一步的分析表明，Ms-Rv3340 中的半胱氨酸-HO 处理通过芬顿反应引发 DNA 损伤。Ms_Rv3340 下调了三个链霉素反应基因的表达水平。据我们所知，以前没有研究报道过 Rv3340 可以产生 HS 调节对链霉素的耐药性，这为结核病的治疗和控制提供了更深入的认识。