Kim Ju-Sim, Sung Moon-Hee, Kho Dhong-Hyo, Lee Jeong K
Department of Life Science and Interdisciplinary Program of Integrated Biotechnology, Sogang University, Seoul 121-742, Korea.
J Bacteriol. 2005 Sep;187(17):5984-95. doi: 10.1128/JB.187.17.5984-5995.2005.
The manganese-containing superoxide dismutase (MnSOD) of Vibrio vulnificus, normally detected after the onset of the stationary phase, is expressed during the lag that immediately follows the transfer of cells grown exponentially to a fresh medium acidified to pH 5.0, whereas Fe-containing SOD is constitutively expressed. The signal triggering the growth lag and MnSOD induction therein is not low pH but intracellular superoxide accumulated under these conditions, since addition of a superoxide scavenger not only shortened the lag but also abrogated the MnSOD induction. If the lysine decarboxylase reaction proceeds in the presence of sufficient lysine, the broth is rapidly neutralized to abolish the generation of oxidative stress. Accordingly, the acid tolerance response was examined without the addition of lysine. SoxR regulates MnSOD induction. Lack of MnSOD caused by mutations in soxR or sodA resulted in low tolerance to low pH. The fur mutant derepressing MnSOD showed better tolerance than the wild type. Thus, an increase in total cytosolic SOD activity through MnSOD induction is essential for the cell to withstand the acid challenge. The contribution of cuprozinc-containing SOD to acid tolerance is not significant compared with those of cytosolic SODs.
创伤弧菌含锰超氧化物歧化酶(MnSOD)通常在稳定期开始后被检测到,在指数生长期的细胞转移至酸化至pH 5.0的新鲜培养基后紧接着的延迟期内表达,而含铁超氧化物歧化酶(Fe-SOD)则是组成型表达。引发生长延迟及其中MnSOD诱导的信号并非低pH,而是在这些条件下积累的细胞内超氧化物,因为添加超氧化物清除剂不仅缩短了延迟期,还消除了MnSOD的诱导。如果赖氨酸脱羧酶反应在有足够赖氨酸存在的情况下进行,肉汤会迅速中和以消除氧化应激的产生。因此,在不添加赖氨酸的情况下检测了酸耐受性反应。SoxR调节MnSOD的诱导。soxR或sodA突变导致的MnSOD缺失导致对低pH的耐受性降低。去阻遏MnSOD的fur突变体比野生型表现出更好的耐受性。因此,通过MnSOD诱导增加总胞质超氧化物歧化酶活性对于细胞耐受酸挑战至关重要。与胞质超氧化物歧化酶相比,含铜锌超氧化物歧化酶对酸耐受性的贡献不显著。