Yamada K, Ono T, Nishioka H
Biosystem Research Laboratory, Faculty of Engineering, Doshisha University, Kyoto, Japan.
J Radiat Res. 1996 Mar;37(1):29-37. doi: 10.1269/jrr.37.29.
Escherichia coli mutants which lack defence systems against such active oxygen forms as OxyR (delta oxyR), superoxide dismutase (SOD) (sodA and sodB) and catalase (katE and katG) are sensitive to UV-A lethality under aerobic conditions, whereas OxyR- and SOD-mutants have resistance under anaerobic conditions and in the presence of sodium azide (NaN3) during irradiation. UV-A induces lipid peroxidation in the delta oxyR mutant, which is suppressed by NaN3. These results suggest that UV-A generates 1O2 or the hydroxyl radical to produce lipid peroxides intracellularly in the delta oxyR mutant and that O2- stress may be generated in the sodAB mutant after 8hr of exposure to UV-A. The sensitivities of such DNA repair-deficient mutants as recA(ind-) and uvrA to UV-A also were examined and compared. These mutants are sensitive to UV-A lethality under aerobic conditions but show only slight resistance under anaerobic conditions or in the presence of NaN3 during irradiation. We conclude that NaN3 protects these mutant cells from oxygen-dependent UV-A lethality.
缺乏针对诸如OxyR（ΔoxyR）、超氧化物歧化酶（SOD）（sodA和sodB）以及过氧化氢酶（katE和katG）等活性氧形式的防御系统的大肠杆菌突变体，在有氧条件下对UV-A致死作用敏感，而OxyR和SOD突变体在厌氧条件下以及在辐照期间存在叠氮化钠（NaN₃）时具有抗性。UV-A在ΔoxyR突变体中诱导脂质过氧化，这被NaN₃所抑制。这些结果表明，UV-A在ΔoxyR突变体中产生单线态氧（¹O₂）或羟基自由基以在细胞内产生脂质过氧化物，并且在暴露于UV-A 8小时后，sodAB突变体中可能产生超氧阴离子（O₂⁻）应激。还检查并比较了诸如recA（ind-）和uvrA等DNA修复缺陷突变体对UV-A的敏感性。这些突变体在有氧条件下对UV-A致死作用敏感，但在厌氧条件下或在辐照期间存在NaN₃时仅表现出轻微抗性。我们得出结论，NaN₃保护这些突变细胞免受依赖氧气的UV-A致死作用。
