Effect of endocrine disruptor para-nonylphenol on the cell growth and oxygen radical generation in Escherichia coli mutant cells deficient in catalase and superoxide dismutase
Effect of endocrine disruptor para-nonylphenol on the cell growth and oxygen radical generation in Escherichia coli mutant cells deficient in catalase and superoxide dismutase
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DOI：
10.1016/j.freeradbiomed.2004.07.001
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发表时间：
2004-11-01
影响因子：
7.4
通讯作者：
Inoue, M
中科院分区：
文献类型：
--
作者：
Okai, Y;Sato, EF;Inoue, M
对壬基酚（NP）对细菌和酵母细胞的生长有很强的抑制作用，这些作用与NP诱导的自由基氧（ROS）的产生有关。在本研究中，我们确定野生型大肠杆菌（CSH 7、SY-11和IFO-3545）与之前报道的其他敏感微生物相比，对NP具有耐药性。为了更详细地阐明NP诱导的ROS生成与细胞生长抑制之间的关系，我们分析了NP对缺乏过氧化氢酶和超氧化物歧化酶（SOD）等ROS清除酶的野生型和突变型大肠杆菌菌株的细胞生长和存活的影响。sod缺陷菌株QC 774 （sod A（-）和sod B-）对NP的敏感性明显高于野生型（CSH 7）和过氧化氢酶缺陷菌株（um1 kat E-和kat G(-)）。作为比较实验，当过氧化氢应用于相同的生长和存活试验时，UM I细胞比QC 774和CSH 7对过氧化氢更敏感。用MCLA（2-甲基-6-[f-甲基苯基]-3,7-二氢咪唑[1,2- α]吡嗪-3- 1）进行的化学发光（CHL）实验显示，NP在QC 774细胞中引起了明显的CHL生成，但在CSH 7和UM 1细胞中没有引起。然而，使用主要反映羟基自由基和次氯酸盐的L-012进行CHL实验，在相同浓度的NP下，QC 774细胞中没有明显的CHL生成。此外，添加SOD可以阻止np诱导的ROS生成和抑制QC 774细胞的存活，但过氧化氢酶和金属螯合剂去铁胺没有显著作用。这些结果表明，NP在细胞中的主要作用之一是产生超氧化物，这可能是NP诱导细胞生长抑制的原因。(C) 2004爱思唯尔公司版权所有。
para-Nonylphenot (NP) had previously been found to have strong suppressive effects of growth of bacterial and yeast cells, and these effects were associated with NP-induced generation of radical oxygen species (ROS). In the present study, we determined that wild-type strains of Escherichia coli (CSH 7, SY-11, and IFO-3545) were resistant to NP compared with other sensitive microorganisms reported previously. To elucidate the relationship between NP-induced ROS generation and cell growth inhibition in more detail, we analyzed the effect of NP on cell growth and survival of wild-type and mutant E. coli strains deficient in ROS-scavenging enzymes such as catalase and superoxide dismutase (SOD). The SOD-deficient strain QC 774 (sod A(-) and sod B-) was much more sensitive to NP than wild-type (CSH 7) and catalase-deficient (UM 1 kat E- and kat G(-)) strains. As a comparative experiment, when hydrogen peroxide was applied to the same growth and survival assays, UM I cells were more sensitive to hydrogen peroxide than QC 774 and CSH 7. A chemiluminescence (CHL) experiment using MCLA (2-methyl-6-[f-methylphenyl]-3,7-dihydroimidazc [1,2-alpha] pyrazin-3-one) reflecting predominantly superoxide generation showed that NP caused marked CHL generation in QC 774 cells, but not in CSH 7 and UM 1 cells. However, the CHL experiment using L-012 reflecting predominantly hydroxyl radical and hypochlorite did not exhibit significant CHL generation in QC 774 cells at the same concentrations of NP. Furthermore, supplementation with SOD prevented NP-induced ROS generation and cell survival inhibition of QC 774 cells, but the catalase and metal-chelating agent deferoxamine did not have significant effects. These results suggest that one of the primary actions of NP in cells is the generation of superoxide which may be responsible for NP-induced cell growth inhibition. (C) 2004 Elsevier Inc. All rights reserved.