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Mycobacterium tuberculosis metC (Rv3340) derived hydrogen sulphide conferring bacteria stress survival

机译:结核分枝杆菌METC(RV3340)衍生的硫化氢赋予细菌胁迫生存

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摘要

Tuberculosis, especially multidrug resistant cases, remains an enormous public health threat. Mycobacterium tuberculosis metC (Rv3340) an enzyme involved in methionine biosynthesis was identified and characterised for antimicrobial susceptibility. We reported that the overexpression of Rv3340 in Mycobacterium smegmatis (Ms_Rv3340) produces hydrogen sulphide (H_2S) for its energy in harsh conditions. The produced H_2S sustained Ms_Rv3340 against streptomycin, whereas the chemical inhibition of H_2S caused streptomycin lethality to Ms_Rv3340. Further analysis showed that cysteine-H_2O_2 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 M. tuberculosis metC (Rv3340) can generates H_2S modulating resistant to streptomycin which provides a greater perception toward the treatment and control of tuberculosis.
机译:结核病,特别是多药抵抗案件,仍然是一个巨大的公共卫生威胁。 结核病患者(RV3340)鉴定了蛋氨酸生物合成中涉及的酶,并表征抗微生物敏感性。 我们报道称,SMEGMATIS(MS_RV3340)中RV3340的过表达在恶劣的条件下产生硫化氢(H_2S)。 所生产的H_2S对链霉素持续MS_RV3340,而H_2S的化学抑制导致链霉素致死至MS_RV3340。 进一步的分析表明,通过芬顿反应将MS-RV3340的半胱氨酸-H_2O_2治疗已引发DNA损伤。 MS_RV3340下调三种链霉素敏感基因的表达水平。 据我们所知,先前没有研究过核心结核病(RV3340)可以产生调节对链霉素的抗性的H_2S,这提供了对治疗和控制结核病的影响。

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