Rifamycin S, a quinone antibiotic, targets Gram-positive bacteria (including MRSA). It represents the oxidized form of a reversible oxidation-reduction system involving two electrons. Rifamycin S generates reactive oxygen species (ROS) and impedes microsomal lipid peroxidation. It finds utility in the treatment of tuberculosis and leprosy [1][2][3].
体内研究
Rat liver sub-mitochondrial particles produce hydroxyl radicals when exposed to NADH and Rifamycin S, with NADH dehydrogenase (complex I) playing a key role in Rifamycin S reduction. NADH is nearly as effective as NADPH in catalyzing the interaction of these antibiotics with rat liver microsomes. Rifamycin S undergoes reduction to Rifamycin SV, a hydroquinone, by Fe(II), forming a detectable Fe(II)-(Rifamycin S)3 complex. Rifamycin S inhibits Fe:ATP-induced lipid peroxidation completely. It undergoes redox-cycling with rat liver microsomes, leading to hydroxyl radical production in the presence of iron complexes [1].
体外研究
The bacteriostatic effect of Rifamycin SV stems from the generation of active oxygen species through its oxidation-reduction cycle within cells. Metal ions, including Mn2+, Cu2+, and Co2+, induce the aerobic oxidation of Rifamycin SV to Rifamycin S, with Mn2+ being the most potent catalyst [2].
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