The antibiotic ceftazidime is a singlet oxygen quencher as demonstrated by ultra-weak chemiluminescence and by inhibition of AAP consumption
The antibiotic ceftazidime is a singlet oxygen quencher as demonstrated by ultra-weak chemiluminescence and by inhibition of AAP consumption
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DOI：
10.1016/s0304-4165(97)00083-4
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发表时间：
1998-01-08
影响因子：
3
通讯作者：
Lamy, M
中科院分区：
文献类型：
--
作者：
Deby-Dupont, G;Deby, C;Lamy, M
我们证明了头孢菌素抗生素头孢他啶（CAZ）使单线态氧（O-1（2））失活。研究了CAZ对Mallet反应（H_2O_2 + HOCl ~-> HCl + H_2O + O ~（-1）（2））产生的O ~（-1）（2）能量衰减相关的超弱化学发光（uwCL）和对虎红（RE）照射产生的O ~（-1）（2）消耗蒽-9，10-二丙酸（AAP）的影响机制。通过CAZ扩增（6.2倍）由Mallet反应产生的uwCL。使用红色和蓝色滤光片，分别吸收610 nm以下和470 - 700 nm之间的辐射，表明CAZ通过波长短于O-1的633和704 nm波长发射的辐射发射增加uwCL（2）。CAZ通过清除过量的O-1（2）的能量而被激发，使O-1（2）回复到基态，而CAZ通过430-480 nm的光发射而失活，CAZ还以剂量依赖的方式抑制RE照射产生的O-1（2）对AAP的消耗。5 × 10（-3）M CAZ对AAP的保护作用相当于10（-3）M组氨酸和3 × 10（-6）M叠氮化钠。这种O-1（2）失活过程将用于特征为PMN过度活化并释放活性氧的疾病。(C)1998年Elsevier Science B.V.
We demonstrated that the cephalosporin antibiotic ceftazidime (CAZ) deactivated singlet oxygen (O-1(2)). We then studied the mechanisms of the CAZ effects on the ultra weak chemiluminescence (uwCL) associated with the energy decay of O-1(2) generated by the Mallet reaction (H2O2 + HOCl --> HCl + H2O + O-1(2)), and on the anthracene-9,10-dipropionic acid (AAP) consumption by O-1(2) generated by irradiation of Rose Bengal (RE). The uwCL generated by the Mallet reaction was amplified (6.2 times) by CAZ. The use of red and blue filters, which absorb radiation below 610 nm and between 470 and 700 nm respectively, demonstrated that CAZ increased the uwCL by a radiation emission at wavelengths shorter than the 633 and 704 nm wavelength emissions of O-1(2). CAZ was excited by scavenging the energy excess of O-1(2), which so returned to its fundamental state, while CAZ deactivated with light emission between 430-480 nm, CAZ also inhibited in a dose-dependent manner the consumption of AAP by O-1(2) generated by the irradiation of RE. The protection of AAP by 5 x 10(-3) M CAZ was equivalent to that of 10(-3) M histidine and 3 x 10(-6) M sodium azide. This process of O-1(2) deactivation will be useful in diseases characterized by an excessive PMN activation with a release of activated oxygen species. (C) 1998 Elsevier Science B.V.