Sulfite-mediated oxidative stress in kidney cells

Vincent, Annette S.; Lim, Bee-Gim; Tan, Jasmine; Whiteman, Matthew; Cheung, Nam Sang; Halliwell, Barry; Wong, Kim Ping

doi:10.1111/j.1523-1755.2004.00391.x

Cited by 52 publications

(36 citation statements)

References 50 publications

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“…2). Similar observations have been reported with rat kidney mitochondria and MDCKII and OK cells (30). However, when other respiratory substrates, namely ␣-ketoglutarate, malate, and succinate, were added at concentrations that mimic their relative concentrations in the whole rat/mouse brain, the inhibitory effect of sulfite on ATP production was not shown (Table III).…”

Section: Discussionsupporting

confidence: 61%

“…The measurement of intracellular ATP was based on the luciferin-luciferase reaction. Both methods have been reported in our previous study (30).…”

Section: Methodsmentioning

confidence: 99%

“…In this study, we examined the effects of SO 3 2Ϫ on rat brain mitochondria and Neuro-2a and PC12 cells and attempted to elucidate its mechanism of action following our earlier observation that micromolar concentrations of SO 3 2Ϫ produced an increase in reactive oxygen species (ROS) in Madin-Darby canine kidney (MDCK) and opossum kidney (OK) cells. The sulfite-mediated oxidative stress was accompanied by a depletion of intracellular ATP, and this was thought to be due to its inhibitory action on mitochondrial glutamate dehydrogenase (30).…”

mentioning

confidence: 99%

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A Mechanism of Sulfite Neurotoxicity

Zhang

Vincent

Halliwell

et al. 2004

Journal of Biological Chemistry

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126

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Exposure of Neuro-2a and PC12 cells to micromolar concentrations of sulfite caused an increase in reactive oxygen species and a decrease in ATP. Likewise, the biosynthesis of ATP in intact rat brain mitochondria from the oxidation of glutamate was inhibited by micromolar sulfite. Glutamate-driven respiration increased the mitochondrial membrane potential (MMP), and this was abolished by sulfite but the MMP generated by oxidation of malate and succinate was not affected. The increased rate of production of NADH from exogenous NAD ؉ and glutamate added to rat brain mitochondrial extracts was inhibited by sulfite, and mitochondria preincubated with sulfite failed to reduce NAD ؉ . Glutamate dehydrogenase (GDH) in rat brain mitochondrial extract was inhibited dose-dependently by sulfite as was the activity of a purified enzyme. An increase in the K m (glutamate) and a decrease in V max resulting in an attenuation in V max /K m (glutamate) at 100 M sulfite suggest a mixed type of inhibition. However, uncompetitive inhibition was noted with decreases in both K m (NAD ؉ ) and V max , whereas V max /K m (NAD ؉ ) remained relatively constant. We propose that GDH is one target of action of sulfite, leading to a decrease in ␣-ketoglutarate and a diminished flux through the tricarboxylic acid cycle accompanied by a decrease in NADH through the mitochondrial electron transport chain, a decreased MMP, and a decrease in ATP synthesis. Because glutamate is a major metabolite in the brain, inhibition of GDH by sulfite could contribute to the severe phenotype of sulfite oxidase deficiency in human infants.

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Section: Discussionsupporting

confidence: 61%

“…The measurement of intracellular ATP was based on the luciferin-luciferase reaction. Both methods have been reported in our previous study (30).…”

Section: Methodsmentioning

confidence: 99%

mentioning

confidence: 99%

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A Mechanism of Sulfite Neurotoxicity

Zhang

Vincent

Halliwell

et al. 2004

Journal of Biological Chemistry

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126

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“…In neurons and human fetal liver cells, it has also been shown that ATP is depleted due to sulfite toxicity [9]. Similar observations were made in rat kidney mitochondria and other nonneuronal cells [85]. In addition, it has been shown that sulfite inhibits mitochondrial glutamate dehydrogenase activity [9].…”

Section: Discussionsupporting

confidence: 61%

Sulfite Oxidase Activity of Cytochrome C: Role of Hydrogen Peroxide

Murugesan

Hemann

Cardounel

et al. 2015

Free Radical Biology and Medicine

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“…17 The buffer used consisted of 100 mmol/L KCl, 12.5 mmol/L KH 2 PO 4 , and 10 mmol/L Tris, pH 7.6. A total of 0.03 mg cortical mitochondria (nϭ6) was incubated with 1 mL of buffer and 125 mol/L adenosine diphosphate, complex II substrate 10 mmol/L succinate, complex I inhibitor 5 mol/L rotenone, and the presence or absence of studied drugs with or without H 2 O 2 under condition of continual shaking for 5 minutes at 24°C.…”

Section: Atp Biosynthesis In Isolated Mitochondriamentioning

confidence: 99%

Leonurine Protects Middle Cerebral Artery Occluded Rats Through Antioxidant Effect and Regulation of Mitochondrial Function

Loh

Jia

Tan

et al. 2010

Stroke

130

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Background and Purpose-Oxidative stress is known to be involved in ischemic stroke. Intense interest is drawn to the therapeutic potential of Chinese herbs on ischemic stroke because many of them contain antioxidant properties. Leonurine, 1 of the active compounds from purified Herba Leonuri, was studied to evaluate its possible therapeutic effects on ischemic stroke. Method-Middle cerebral artery occlusion was selected as our model of study. The animals were pretreated with Leonurine orally for 7 days and the surgery was done. One day after surgery, 2,3,5-triphenyltetrazolium chloride staining and neurological deficit score were carried out to evaluate the functional outcome of animals, whereas levels of superoxide dismutase, glutathione peroxidase, and malondialdehyde were analyzed for oxidative stress analysis. For mitochondrial studies, 3 hours after surgery, mitochondria were isolated for analysis of reactive oxygen species production, adenosine triphosphate biosynthesis, oxygen consumption, and respiratory control ratio value. Result-In in vivo experiments, Leonurine pretreatment reduced infarct volume, improved neurological deficit in stroke groups, increased activities of antioxidant enzymes superoxide dismutase and glutathione peroxidase, and decreased levels from the lipid peroxidation marker malondialdehyde. In terms of mitochondrial modulation, Leonurine inhibited mitochondrial reactive oxygen species production and adenosine triphosphate biosynthesis. Animal studies also demonstrated that the mitochondrial function and redox state were restored by Leonurine treatment. Conclusions-Leonurine has neuroprotective effects and carries a therapeutic potential of stroke prevention. (Stroke.

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Sulfite-mediated oxidative stress in kidney cells

Cited by 52 publications

References 50 publications

A Mechanism of Sulfite Neurotoxicity

A Mechanism of Sulfite Neurotoxicity

Sulfite Oxidase Activity of Cytochrome C: Role of Hydrogen Peroxide

Leonurine Protects Middle Cerebral Artery Occluded Rats Through Antioxidant Effect and Regulation of Mitochondrial Function

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