The formation of carbon centered free radicals, identified as methylcarbonyl species, was observed using ESR spectroscopy and the spin trapping agent 4-pyridyl-1-oxide-N-t-butyl nitrone (4-POBN) during the oxidation of acetaldehyde by xanthine oxidase. The reaction was dependent upon the presence of OH* radicals and was inhibited by the addition of superoxide dismutase, catalase or OH* radical scavengers. The generation of methylcarbonyl radicals was associated with a doubling of stable acetaldehyde adducts with serum albumin, and 4-POBN or superoxide dismutase and catalase, completely blocked this effect. Thus, methylcarbonyl radicals contributed to acetaldehyde-mediated protein alkylation which is involved in causing toxic as well as immunological reactions ascribed to acetaldehyde.
FREE-RADICAL ACTIVATION OF ACETALDEHYDE AND ITS ROLE IN PROTEIN ALKYLATION / Albano, E; Clot, P; Comoglio, A; Dianzani, Mu; Tomasi, Aldo. - In: FEBS LETTERS. - ISSN 0014-5793. - STAMPA. - 348:(1994), pp. 65-69.
FREE-RADICAL ACTIVATION OF ACETALDEHYDE AND ITS ROLE IN PROTEIN ALKYLATION
TOMASI, Aldo
1994-01-01
Abstract
The formation of carbon centered free radicals, identified as methylcarbonyl species, was observed using ESR spectroscopy and the spin trapping agent 4-pyridyl-1-oxide-N-t-butyl nitrone (4-POBN) during the oxidation of acetaldehyde by xanthine oxidase. The reaction was dependent upon the presence of OH* radicals and was inhibited by the addition of superoxide dismutase, catalase or OH* radical scavengers. The generation of methylcarbonyl radicals was associated with a doubling of stable acetaldehyde adducts with serum albumin, and 4-POBN or superoxide dismutase and catalase, completely blocked this effect. Thus, methylcarbonyl radicals contributed to acetaldehyde-mediated protein alkylation which is involved in causing toxic as well as immunological reactions ascribed to acetaldehyde.
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