Bogdanov P M, Bertorello M M, Albesa I
Departamento de Farmacia, Facultad de Ciencias Químicas, Universidad Nacional de Córdoba, Argentina.
Biochem Biophys Res Commun. 1998 Mar 17;244(2):561-6. doi: 10.1006/bbrc.1997.8109.
Staphylococcus aureus was inhibited by exposure to 2-hydroxy-N-(3,4-dimethyl-5-isoxazolyl)-1,4-naphthoquinone-4-imine (Q1). This compound was cleavaged in the presence of bacteria and an efflux of isoxazolamine was detected whereas in the S. aureus membrane and cytoplasm was observed an absorption band similar to that of the bencenoid ring. Non-viable bacteria showed intact Q1 intracellularly and in the membrane. Antistaphylococcus effect was associated to Q1 interaction with the respiratory chain, the oxidative metabolites were stimulated; there was cellular injury simultaneous to reduction of antibiotic molecule and efflux of isoxazolamine. The bacteria treated with Q1 increased its oxygen consumption and superoxide anion generation. Superoxide dismutase (SOD) production was stimulated, but it was principally extracellular in S. aureus. Escherichia coli, a species resistant to the antibiotic, did not reduce Q1 and showed lower superoxide anion generation; besides, there was an increase of intracellular SOD with extracellular decrease.
金黄色葡萄球菌在接触2-羟基-N-(3,4-二甲基-5-异恶唑基)-1,4-萘醌-4-亚胺（Q1）时受到抑制。该化合物在细菌存在的情况下会发生裂解，并检测到异恶唑胺的流出，而在金黄色葡萄球菌的细胞膜和细胞质中观察到与苯环类似的吸收带。无活力的细菌在细胞内和细胞膜中显示Q1完整无损。抗葡萄球菌作用与Q1与呼吸链的相互作用有关，氧化代谢产物受到刺激；在抗生素分子还原和异恶唑胺流出的同时存在细胞损伤。用Q1处理的细菌增加了其耗氧量和超氧阴离子的产生。超氧化物歧化酶（SOD）的产生受到刺激，但在金黄色葡萄球菌中主要存在于细胞外。大肠杆菌是一种对该抗生素耐药的菌种，它不会还原Q1，超氧阴离子的产生较低；此外，细胞内SOD增加而细胞外SOD减少。
