Sulfate anion free radical formation by the peroxidation of (Bi) sulfite and its reaction with hydroxyl radical scavengers

Mottley, Carolyn; Mason, Ronald P.

doi:10.1016/0003-9861(88)90077-x

Cited by 131 publications

(117 citation statements)

References 44 publications

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“…1A). The hyperfine coupling constants of the assigned DMPO/ ⅐ SO 3 Ϫ radical adduct (a N ϭ 14.7 G and a ␤ H ϭ 16.0 G) are consistent with previous reports (9,15). When EPO, bisulfite, or H 2 O 2 was omitted, no radical adduct was formed ( Fig.…”

Section: Esr Optical Spectroscopy and Oxygen Uptake-incubationssupporting

confidence: 91%

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Protein Radical Formation Resulting from Eosinophil Peroxidase-catalyzed Oxidation of Sulfite

Ranguelova

Chatterjee

Ehrenshaft

et al. 2010

Journal of Biological Chemistry

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Section: Esr Optical Spectroscopy and Oxygen Uptake-incubationssupporting

confidence: 91%

“…The oxygen transfer reaction of Ϫ O 3 SOO ⅐ to form SO 4 . is a general reaction of peroxyl radicals and is not limited to oxygen donation to sulfite as in Reaction 7 (2,14,15). Furthermore, SO 4 .…”

mentioning

confidence: 99%

Protein Radical Formation Resulting from Eosinophil Peroxidase-catalyzed Oxidation of Sulfite

Ranguelova

Chatterjee

Ehrenshaft

et al. 2010

Journal of Biological Chemistry

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“…To prevent this, 2.0 mM DETAPAC was added to all of the reaction mixtures, following Mottley and Mason [19]. As may be noted from Fig.…”

Section: So'j-generation From So~-by Xanthine Oxidase/homentioning

confidence: 99%

“…Indeed, the amount of SO;-generated was found to ing ~ As (e) but inactivated X.O. SO;-adduct formed in other systems [11,13,17,19,[22][23][24][25], demonstrating the formation of the SO;-radical in the reaction mixture. Omission of any one component caused a dramatic decrease in SO~" generation (Fig.…”

Section: So'j-generation From So~-by Xanthine Oxidase/homentioning

confidence: 99%

“…Third, we noted that while the mechanism of SO;-generation from SOl-via autoxidation and trace-metal catalyzed oxidation has been studied in detail [10][11][12][13][14], relatively little is known about the mechanism of SO;-generation through enzymatic pathway, with the exception of some recent studies [15][16][17][18][19]. In particular, Mason and coworkers [17][18][19] utilized ESR and ESR spin trap methodology to identify SO;-formation during the prostaglandin/hydroperoxidase-catalyzed oxidation of SOl- [17,18], and SO;-/SO]-radical formation during SOl-oxidation by peroxidase/H,.O~ [19]. …”

Section: Introductionmentioning

confidence: 99%

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Xanthine oxidase/hydrogen peroxide generates sulfur trioxide anion radical (SO^.−₃) from sulfite (SO²⁻₃)

1992

FEBS Letters

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In the presence of hydrogen peroxide (H20:), xanthine oxidase has been found to catalyze sulfur trioxide anion radical (SO;-) formation from sullite anion (SO]-), The SO]" radical was identified by ESR (electron spin resonance) spin trapping, utilizing 5,5-dimethyl-l-pyrroline-l-oxide (DMPO) as the spin trap, Inactivated xanthin~ oxidase does not catalyze SO;-radical formation, implying a specific role for this enzyme. The initial rate ofSO]-radical formation increases linearly with xanth ine oxidasc concentration, To~ethcr, thes¢ observations indicate that the $07 generation occurs enzymatic.ally. These results suggest a new property of xanthine oxidase and perhaps also a significant step in the m~hanism of sulfitc toxicity in cellular systems.

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The mitochondrial‐targeted reactive species scavenger JP4‐039 prevents sulfite‐induced alterations in antioxidant defenses, energy transfer, and cell death signaling in striatum of rats

Glänzel

Grings

Rosa-Junior

et al. 2020

J of Inher Metab Disea

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Sulfite oxidase (SO) deficiency is a disorder caused either by isolated deficiency of SO or by defects in the synthesis of its molybdenum cofactor. It is characterized biochemically by tissue sulfite accumulation. Patients present with seizures, progressive neurological damage, and basal ganglia abnormalities, the pathogenesis of which is not fully established. Treatment is supportive and largely ineffective. To address the pathophysiology of sulfite toxicity, we examined the effects of intrastriatal administration of sulfite in rats on antioxidant defenses, energy transfer, and mitogen‐activated protein kinases (MAPK) and apoptosis pathways in rat striatum. Sulfite administration decreased glutathione (GSH) concentration and glutathione peroxidase, glucose‐6‐phosphate dehydrogenase, glutathione S‐transferase, and glutathione reductase activities in striatal tissue. Creatine kinase (CK) activity, a crucial enzyme for cell energy transfer, was also decreased by sulfite. Superoxide dismutase‐1 (SOD1) and catalase (CAT) proteins were increased, while heme oxygenase‐1 (HO‐1) was decreased. Additionally, sulfite altered phosphorylation of MAPK by decreasing of p38 and increasing of ERK. Sulfite further augmented the content of GSK‐3β, Bok, and cleaved caspase‐3, indicating increased apoptosis. JP4‐039 is a mitochondrial‐targeted antioxidant that reaches higher intramitochondrial levels than other traditional antioxidants. Intraperitoneal injection of JP4‐039 before sulfite administration preserved activity of antioxidant enzymes and CK. It also prevented or attenuated alterations in SOD1, CAT, and HO‐1 protein content, as well as changes in p38, ERK, and apoptosis markers. In sum, oxidative stress and apoptosis induced by sulfite injection are prevented by JP4‐039, identifying this molecule as a promising candidate for pharmacological treatment of SO‐deficient patients.

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Sulfate anion free radical formation by the peroxidation of (Bi) sulfite and its reaction with hydroxyl radical scavengers

Cited by 131 publications

References 44 publications

Protein Radical Formation Resulting from Eosinophil Peroxidase-catalyzed Oxidation of Sulfite

Protein Radical Formation Resulting from Eosinophil Peroxidase-catalyzed Oxidation of Sulfite

Xanthine oxidase/hydrogen peroxide generates sulfur trioxide anion radical (SO^.−₃) from sulfite (SO²⁻₃)

The mitochondrial‐targeted reactive species scavenger JP4‐039 prevents sulfite‐induced alterations in antioxidant defenses, energy transfer, and cell death signaling in striatum of rats

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Sulfate anion free radical formation by the peroxidation of (Bi) sulfite and its reaction with hydroxyl radical scavengers

Cited by 131 publications

References 44 publications

Protein Radical Formation Resulting from Eosinophil Peroxidase-catalyzed Oxidation of Sulfite

Protein Radical Formation Resulting from Eosinophil Peroxidase-catalyzed Oxidation of Sulfite

Xanthine oxidase/hydrogen peroxide generates sulfur trioxide anion radical (SO.−3) from sulfite (SO2−3)

The mitochondrial‐targeted reactive species scavenger JP4‐039 prevents sulfite‐induced alterations in antioxidant defenses, energy transfer, and cell death signaling in striatum of rats

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Xanthine oxidase/hydrogen peroxide generates sulfur trioxide anion radical (SO^.−₃) from sulfite (SO²⁻₃)