Redox Cycling of Polycyclic Aromatic Hydrocarbono-Quinones: Reversal of Superoxide Dismutase Inhibition by Ascorbate

Jarabak, Rebecca; Harvey, Ronald G.; Jarabak, Joseph

doi:10.1006/abbi.1996.9858

Cited by 20 publications

(12 citation statements)

References 33 publications

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“…Molecular oxygen is consumed with hydrogen peroxide formation during induction period according to reaction (16) of Scheme . The same was shown elsewhere 26. It has been found in our tests that the oxygen consumption rates during p ‐QH 2 , PG, PK, and 4CH 3 ‐PK oxidations with AscH 2 are lower than the corresponding rates of these oxidations without inhibitor, but induction period is completely absent, that is, observation of the system by only oxygen consumption does not allow us to find the time of full inhibitor exhaustion.…”

Section: Resultssupporting

confidence: 85%

“…Thus, for determining the radical reaction initiation rate we examined l ‐ascorbic acid as an inhibitor. This substance reduces phenoxyl radicals and quinones to phenols, and oxygen‐centered radicals to hydrogen peroxide (see scheme ) 25–27. So, as long as the system contains ascorbic acid the phenol will not be consumed, nor will quinone be accumulated.…”

Section: Resultsmentioning

confidence: 99%

“…Thus, taking into account references data 20,22,23,25–28 and obtained experimental results, the phenol oxidation process by molecular oxygen in alkaline aqueous media with AscH 2 inhibition can be presented as in Scheme 1, where QH 2 is polyphenol, AscH − is ascorbate‐anion form of l ‐ascorbic acid, Q • is semiquinone, Asc • is ascorbic‐radical anion, dAsc is l ‐dehydroascorbic acid, Q* is quinone in electron‐excited state.…”

Section: Resultsmentioning

confidence: 99%

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Radical formation during phenol oxidation in aqueous media

Shendrik

Odaryuk

Kanibolotska

et al. 2012

Int J of Chemical Kinetics

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Kinetics of oxygen consumption, reaction product formation, and chemiluminescence during polyphenol oxidation by molecular oxygen in alkaline aqueous media with additions of L-ascorbic acid (AscH 2 ) and homocysteine (HCys) has been investigated. In these processes, AscH 2 and HCys have been shown to act as typical radical-reaction inhibitors that can be used for determinations of the radical formation rates. The rates of radical formation during oxidation of hydroquinone ( p-QH 2 ), chlorohydroquinone (Cl-QH 2 ), 2,5-dichlorohydroquinone (2,5Cl-QH 2 ), catechol (PK), 4-methylcatechol (4CH 3 -PK), pyrogallol (PG), gallic acid (GK) have been estimated.

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Section: Resultssupporting

confidence: 85%

Section: Resultsmentioning

confidence: 99%

Section: Resultsmentioning

confidence: 99%

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Radical formation during phenol oxidation in aqueous media

Shendrik

Odaryuk

Kanibolotska

et al. 2012

Int J of Chemical Kinetics

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“…The toxicity of quinones, such as PHQ, may be due in part to redox cycling (Jarabak et al, 1996(Jarabak et al, , 1997. PHQ can be reduced by enzymes such as NADPH cytochrome P450 reductase, yielding the semiquinone radical (Hasspieler and Di Giulio, 1994).…”

Section: Introductionmentioning

confidence: 99%

Assessment of mixture toxicity of copper, cadmium, and phenanthrenequinone to the marine bacterium Vibrio fischeri

Wang

Lampi

Huang

et al. 2008

Environmental Toxicology

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Transition metals and polycyclic aromatic hydrocarbons (PAHs) are cocontaminants at many sites. Contaminants in mixtures are known to interact with biological systems in ways that can greatly alter the toxicity of individual compounds. The toxicities (individually and as mixtures) of copper (Cu), a redox-active metal; cadmium (Cd), a nonredox active metal; and phenanthrenequinone (PHQ), a redox-active oxygenated PAH, were examined using the bioluminescent bacterium Vibrio fischeri. We found that the cotoxicity of Cu/PHQ was dependent on the ratio of concentrations of each chemical in the mixture. Different interaction types (synergism, antagonism, and additivity) were observed with different combinations of these toxicants. The interaction types changed from antagonism at a low Cu to PHQ ratio (1:4), to additive at an intermediate Cu to PHQ ratio (2:3), to synergistic at higher Cu to PHQ ratios (3:2 and 4:1). In contrast to Cu/PHQ mixtures, the cotoxicity of Cd/PHQ did not change at different mixture ratios and was found for the most part to be additive. For the individual chemicals and their mixtures, reactive oxygen species (ROS) production was observed in V. fischeri, suggesting that individual and mixture toxicity of Cu, Cd, and PHQ to V. fischeri involves ROS-related mechanisms. This study shows that mixture ratios can alter individual chemical toxicity, and should be taken into account in risk assessment.

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“…This finding suggests that ascorbate is acting upstream to remove radical species such as superoxide radicals (Rose and Bode 1993). Ascorbate is known to compete with superoxide dismutase (SOD) for removal of superoxide (Jarabak et al . 1997).…”

Section: Discussionmentioning

confidence: 99%

Cooperative interaction between ascorbate and glutathione during mitochondrial impairment in mesencephalic cultures

Ehrhart¹,

Zeevalk²

2003

Journal of Neurochemistry

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A decrease in total glutathione, and aberrant mitochondrial bioenergetics have been implicated in the pathogenesis of Parkinson's disease. Our previous work exemplified the importance of glutathione (GSH) in the protection of mesencephalic neurons exposed to malonate, a reversible inhibitor of mitochondrial succinate dehydrogenase/complex II. Additionally, reactive oxygen species (ROS) generation was an early, contributing event in malonate toxicity. Protection by ascorbate was found to correlate with a stimulated increase in protein-glutathione mixed disulfide (Pr-SSG) levels. The present study further examined ascorbate-glutathione interactions during mitochondrial impairment. Depletion of GSH in mesencephalic cells with buthionine sulfoximine potentiated both the malonate-induced toxicity and generation of ROS as monitored by dichlorofluorescein diacetate (DCF) fluorescence. Ascorbate completely ameliorated the increase in DCF fluorescence and toxicity in normal and GSH-depleted cultures, suggesting that protection by ascorbate was due in part to upstream removal of free radicals. Ascorbate stimulated Pr-SSG formation during mitochondrial impairment in normal and GSH-depleted cultures to a similar extent when expressed as a proportion of total GSH incorporated into mixed disulfides. Malonate increased the efflux of GSH and GSSG over time in cultures treated for 4, 6 or 8 h. The addition of ascorbate to malonate-treated cells prevented the efflux of GSH, attenuated the efflux of GSSG and regulated the intracellular GSSG/GSH ratio. Maintenance of GSSG/GSH with ascorbate plus malonate was accompanied by a stimulation of Pr-SSG formation. These findings indicate that ascorbate contributes to the maintenance of GSSG/GSH status during oxidative stress through scavenging of radical species, attenuation of GSH efflux and redistribution of GSSG to the formation of mixed disulfides. It is speculated that these events are linked by glutaredoxin, an enzyme shown to contain both dehydroascorbate reductase as well as glutathione thioltransferase activities.

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Redox Cycling of Polycyclic Aromatic Hydrocarbono-Quinones: Reversal of Superoxide Dismutase Inhibition by Ascorbate

Cited by 20 publications

References 33 publications

Radical formation during phenol oxidation in aqueous media

Radical formation during phenol oxidation in aqueous media

Assessment of mixture toxicity of copper, cadmium, and phenanthrenequinone to the marine bacterium Vibrio fischeri

Cooperative interaction between ascorbate and glutathione during mitochondrial impairment in mesencephalic cultures

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