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Title: Ferricytochrome c Directly Oxidizes Aminoacetone to Methylglyoxal, a Catabolite Accumulated in Carbonyl Stress
Authors: Sartori, Adriano [UNIFESP]
Mano, Camila M.
Mantovani, Mariana C. [UNIFESP]
Dyszy, Fabio H.
Massari, Julio
Tokikawa, Rita
Nascimento, Otaciro R.
Nantes, Iseli L.
Bechara, Etelvino José Henriques [UNIFESP]
Universidade de São Paulo (USP)
Universidade Federal de São Paulo (UNIFESP)
Universidade Federal do ABC (UFABC)
Issue Date: 6-Mar-2013
Publisher: Public Library Science
Citation: Plos One. San Francisco: Public Library Science, v. 8, n. 3, 13 p., 2013.
Abstract: Age-related diseases are associated with increased production of reactive oxygen and carbonyl species such as methylglyoxal. Aminoacetone, a putative threonine catabolite, is reportedly known to undergo metal-catalyzed oxidation to methylglyoxal, NH4+ ion, and H2O2 coupled with (i) permeabilization of rat liver mitochondria, and (ii) apoptosis of insulin-producing cells. Oxidation of aminoacetone to methylglyoxal is now shown to be accelerated by ferricytochrome c, a reaction initiated by one-electron reduction of ferricytochrome c by aminoacetone without amino acid modifications. the participation of O-2(center dot-) and HO center dot radical intermediates is demonstrated by the inhibitory effect of added superoxide dismutase and Electron Paramagnetic Resonance spin-trapping experiments with 5,5'-dimethyl-1-pyrroline-N-oxide. We hypothesize that two consecutive one-electron transfers from aminoacetone (E-0 values = -0.51 and -1.0 V) to ferricytochrome c (E-0 = 0.26 V) may lead to aminoacetone enoyl radical and, subsequently, imine aminoacetone, whose hydrolysis yields methylglyoxal and NH4+ ion. in the presence of oxygen, aminoacetone enoyl and O-2(center dot-) radicals propagate aminoacetone oxidation to methylglyoxal and H2O2. These data endorse the hypothesis that aminoacetone, putatively accumulated in diabetes, may directly reduce ferricyt c yielding methylglyoxal and free radicals, thereby triggering redox imbalance and adverse mitochondrial responses.
ISSN: 1932-6203
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