Involvement of oxidative stress in hydroquinone-induced cytotoxicity in catalase-deficient Escherichia coli mutants
Involvement of oxidative stress in hydroquinone-induced cytotoxicity in catalase-deficient Escherichia coli mutants
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DOI：
10.1080/10715760500232008
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发表时间：
2005-10-01
影响因子：
3.3
通讯作者：
Kira, S
中科院分区：
文献类型：
--
作者：
Horita, M;Wang, DH;Kira, S
对苯二酚是一种苯衍生代谢物。为了阐明活性氧（ROS）是否参与了氢醌诱导的细胞毒性，我们构建了大肠杆菌（E。colt）菌株（Cs-b、Cs-c）和野生型（Cs-a）的过氧化氢酶基因。coliUM 255作为受体。过氧化氢酶比活力大小为Cs-a > Cs-c > Cs-b > UM 255，对H2 O2的敏感性大小为UM 255> Cs-b > Cs-c > Cs-a。我们发现，氢醌暴露降低了过氧化氢酶缺陷型大肠杆菌的存活率。大肠杆菌突变株的过氧化氢酶活性随浓度的增加而降低，尤其是过氧化氢酶活性较低的菌株。采用抑菌圈法测定了对苯二酚的毒性，其中UM 255最敏感，生长抑制带最大，其次为Cs-b、Cs-c和Cs-a。此外，我们发现，氢醌诱导的细胞损伤抑制过氧化氢酶，抗坏血酸，二甲基亚砜（DMSO），和乙二胺四乙酸（EDTA）的预处理，并增强超氧化物歧化酶（CuZnSOD和MnSOD）。本研究结果表明，H2 O2可能参与了氢醌诱导的过氧化氢酶缺陷型大肠杆菌细胞毒性。大肠杆菌突变体和过氧化氢酶在保护细胞免受氢醌毒性中起重要作用。
Hydroquinone is a benzene-derived metabolite. To clarify whether the reactive oxygen species (ROS) are involved in hydroquinone-induced cytotoxicity, we constructed transformants of Escherichia coli (E. colt) strains that express mammalian catalase gene derived from catalase mutant mice (Cs-b, Cs-c) and the wild-type (Cs-a) using a catalase-deficient E. coliUM255 as a recipient. Specific catalase activities of these tester strains were in order of Cs-a > Cs-c > Cs-b > UM255, and their susceptibility to hydrogen peroxide (H2O2) showed UM255 > Cs-b > Cs-c > Cs-a. We found that hydroquinone exposure reduced the survival of catalase-deficient E. coli mutants in a dose-dependent manner significantly, especially in the strains with lower catalase activities. Hydroquinone toxicity was also confirmed using zone of inhibition test, in which UM255 was the most susceptible, showing the largest zone of growth inhibition, followed by Cs-b, Cs-c and Cs-a. Furthermore, we found that hydroquinone-induced cell damage was inhibited by the pretreatment of catalase, ascorbic acid, dimethyl sulfoxide (DMSO), and ethylenediaminetetraacetic acid (EDTA), and augmented by superoxide dismutase (both CuZnSOD and MnSOD). The present results suggest that H2O2 is probably involved in hydroquinone-induced cytotoxicity in catalase-deficient E. coli mutants and catalase plays an important role in protection of the cells against hydroquinone toxicity.