Oxidative DNA damage from sulfite autoxidation catalyzed by manganese(III)

Abstract

A series of manganese(II) and manganese(III) salts and oxides were investigated for their ability to catalyze the autoxidation of sulfite resulting in oxidative damage to DNA. Experiments directed at identifying the reactive intermediates responsible for DNA oxidation included the trapping of a sulfite radical adduct during EPR studies, alcohol quenching studies of free radical intermediates, comparisons of relative reactivities toward conversion of Type I to Type II plasmid DNA and cleavage of a duplex DNA restriction fragment. The studies support previous work on the mechanism of manganese(III)-catalyzed sulfite autoxidation and provide evidence that simple manganese salts are capable of mediating substantial DNA damage in conjunction with sulfite.

DNA damage and 2′-deoxyguanosine oxidation induced by S(IV) autoxidation catalyzed by copper(II) tetraglycine complexes: Synergistic effect of a second metal ion

“…In the presence of SO 2À 3 and Cr(VI), the DNA double strand breaks by SO ÅÀ 3 radicals were observed. EPR spectra of SO ÅÀ 3 radical adduct, trapped by DMPO, were also reported by Jameton et al [29] in the autoxidation of SO 2À (8)). …”

“…Studies on DNA damage induced by S(IV) autoxidation in the presence of Mn(II)/ Mn(III)/H 2 O [28,29], Mn(III)/meso-tetrakis(4-N-methylpyridiniumyl)-porphyrinato [28], Cr(VI)/H 2 O [30], Fe(II)/Fe(III)/H 2 O [31,32], Fe(III) and Cu(II)/famotidine [32], Co(II)/H 2 O [33], Ni(II)/lysylglycylhistidine [34], Cu(II)/tetraglycine [35] and Ni(II)/glycylglycylhistidine [36] combined with mechanistic and kinetics data, showed the importance of the balance between oxygen and S(IV) concentrations. Oxysulfur radicals, formed as intermediates in S(IV) autoxidation catalyzed by transition metal ions, have been proposed as key species in DNA damage [25,[29][30][31][32][33][34][35][36][37][38].…”

Influence of copper on the interaction between cytochrome c and sulfite in vitro

“…Human body is exposed to sulfite (SO 2− 3 ) through the inhalation of SO 2 , which is mainly derived from industrial emissions [2], and the ingestion of SO 2− 3 (or HSO 2-3 ) used as a preservative in food [1,3]. The toxic effects associated with sulfite include asthma, mutagenic or conmutagenic effects, and its ability to act as a cocarcinogen [4].…”

“…Although some work had been done about the binding of Cu 2 to Cyt-c [10], the interaction of sulfite and Cu 2 with Cyt-c in a system is still to be reported. So, the studies on the binding of Cu 2 and SO 2− 3 with Cyt-c separately, as well as the influence of Cu 2 on the interaction between sulfite and Cyt-c, may give a better illustration of the interaction between the air pollutant and biomolecules in the human body.…”

Chemiluminescence of cobalt(II)‐catalysed auto‐oxidation of sulphite and its application to cobalt analysis

“…Several studies have indicated that powerful oxidants, such as sulphite radical (SO 3 − · ), sulphate radical (SO 4 − · ), peroxomonosulphate radicals (SO 5 − · ) and peroxomonosulphate (SO 5 2− ) are formed as intermediates in sulphite autoxidation (8,11), and their oxidative damage to cell membranes, proteins and DNA has been investigated (14)(15)(16). In spite of acting as a reducing agent, sulphite is able to induce oxidation of divalent metal ions and complexes to their trivalent state.…”