The catecholic metal sequestering agent 1,2-dihydroxybenzene-3, 5-disulfonate confers protection against oxidative cell damage

Krishna, C. Murali; Liebmann, James; Kaufman, Dwight; DeGraff, William; Hahn, Stephen M.; McMurry, Thomas J.; Mitchell, James B.; Russo, Angelo

doi:10.1016/0003-9861(92)90142-j

Cited by 103 publications

(68 citation statements)

References 39 publications

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“…The spin trap agents tiron, tempol, and PTIYO are effective in vitro scavengers of O 2 ⅐Ϫ , but less potent than SOD or the metal-based SOD mimetics (13,(42)(43)(44). In the present study we showed that none of these compounds shared the ability of Cu/Zn SOD to promote endothelium-dependent relaxation of piglet pulmonary vessels.…”

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confidence: 50%

Role of Superoxide Anion on Basal and Stimulated Nitric Oxide Activity in Neonatal Piglet Pulmonary Vessels

Villamor¹,

Kessels²,

Fischer

et al. 2003

Pediatr Res

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The superoxide anion (O 2 ⅐Ϫ ) appears to be an important modulator of nitric oxide bioavailability. Enzymatic scavenging of O 2 ⅐Ϫ is carried out by superoxide dismutase (SOD). The present study was designed to characterize the developmental changes on pulmonary vascular reactivity induced by 1) exogenous Cu/Zn SOD, 2) several putative SOD mimetics, and 3) endogenous SOD inhibition. We also analyzed age-related changes on pulmonary SOD activity and vascular O 2 ⅐Ϫ levels. SOD (1-300 U/mL) produced endotheliumdependent relaxation of U46619-contracted intrapulmonary arteries (fourth branch) and veins from 12-to 24-h-old and 2-wk-old piglets. SOD-induced relaxation was greater in pulmonary arteries and was abolished by the nitric oxide synthase inhibitor N-nitro-L-arginine methyl ester. SOD induced a greater pulmonary artery relaxation in the 2-wk-old than in the 12-to 24-h-old piglet. SOD (100 U/mL) did not modify acetylcholine-induced relaxation in pulmonary arteries. In contrast, endogenous SOD inhibition by diethyldithiocarbamate (3 mM) impaired acetylcholine-induced relaxation in pulmonary arteries from newborn but not from 2-wk-old piglets. Total SOD activity in lung tissue did not change with postnatal age. With the use of dihydroethidium, an oxidant-sensitive fluorescent probe, we did not find significant age-or vessel-related differences in O 2 Successful adaptation of the newborn to postnatal conditions requires a dramatic transition of the pulmonary circulation from a high-resistance state in utero to a low-resistance state within minutes after birth. Some infants fail to achieve or sustain this normal decrease in pulmonary vascular resistance, which leads to severe respiratory distress and hypoxemia, referred to as PPHN (1) NO ⅐ , a free radical species produced by a wide variety of cell types, has gained recognition as a key mediator of diverse physiologic and pathologic processes, including the regulation of pulmonary vascular tone and the perinatal adaptation of the lung circulation (1).

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Role of Superoxide Anion on Basal and Stimulated Nitric Oxide Activity in Neonatal Piglet Pulmonary Vessels

Villamor¹,

Kessels²,

Fischer

et al. 2003

Pediatr Res

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“…It has been reported that the synthetic seleno-organic compound Ebselen has lipid hydroperoxide-reducing activity (30) and in light of our finding that 7,3-OOH chol is the major oxidized LDL-borne cytotoxin (16), we examined whether Ebselen protects against oxidized LDL induced cell death in human fibroblast cells. (37), Tiron, a well-characterized chelator of intracellular transition metal ions (38), was also tested. Fig.…”

Section: Resultsmentioning

confidence: 99%

“…Many chelators are not exclusively metal scavengers. Under certain circumstances, Tiron may scavenge -OH, superoxide anion, alkyl, and alkoxyl radicals (38) and Desferal may also quench peroxyl radicals (37). We therefore used multiple intracellularly active metal chelators at various concentrations in an attempt to demonstrate more confidently the transition metal involvement in oxidized LDL induced cytotoxicity.…”

Section: Discussionmentioning

confidence: 99%

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In vitro cell injury by oxidized low density lipoprotein involves lipid hydroperoxide-induced formation of alkoxyl, lipid, and peroxyl radicals.

et al. 1995

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Mounting evidence supports current theories linking lipoprotein oxidation to atherosclerosis. We sought the cellular biochemical mechanism by which oxidized LDL inflicts cell injury. Inhibitors of candidate pathways of cell death were used to treat human fibroblast target cells exposed to oxidized LDL. Ebselen, which degrades lipid hydroperoxides, inhibited oxidized LDL toxicity, consistent with our recent report that 7f8-hydroperoxycholesterol (7fi-OOH chol) is the major cytotoxin of oxidized LDL. Intracellular chelation of metal ions inhibited, while preloading cells with iron enhanced, toxicity. Inhibition of oxidized LDL and 7/B-OOH chol toxicity by 2-keto-4-thiolmethyl butyric acid, a putative alkoxyl radical scavenger and by vitamin E, probucol and diphenylphenylenediamine, putative scavengers of peroxyl radicals was consistent with the involvement of these radicals in the lethal sequence. Cell death was thus postulated to occur due to lipid peroxidation via a sequence involving lipid hydroperoxide-induced, iron-mediated formation of alkoxyl, lipid, and peroxyl radicals. Pathways involving other reactive oxygen species, new protein synthesis, or altered cholesterol metabolism were considered less likely, since putative inhibitors failed to lessen toxicity. Understanding the mechanism of cell injury by oxidized LDL and its toxic moiety, 7J3-OOH chol, may indicate specific interventions in the cell injury believed to accompany vascular lesion development. (J. Clin. Invest. 1995Invest. . 96:1866Invest. -1873

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“…When Tiron that inhibited the formation of the WST-1 formazan by the Maillard reaction mixture was present, a characteristic radical (g = 2.0047) was observed in a good accordance with the property of the Tiron radical formed by the reaction with the superoxide anion. 15,16 The signal strength of the Tiron radical was significantly suppressed by the presence of WST-1. This result by the ESR method clearly indicates that the reduction of WST-1 was caused by the 1153 ANALYTICAL SCIENCES OCTOBER 2002, VOL.…”

Section: Comparison Between Wst-1 and Cytochrome C Assaymentioning

confidence: 98%

Spectrophotometric Assay of Superoxide Anion Formed in Maillard Reaction Based on Highly Water-soluble Tetrazolium Salt

et al. 2002

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The catecholic metal sequestering agent 1,2-dihydroxybenzene-3, 5-disulfonate confers protection against oxidative cell damage

Cited by 103 publications

References 39 publications

Role of Superoxide Anion on Basal and Stimulated Nitric Oxide Activity in Neonatal Piglet Pulmonary Vessels

Role of Superoxide Anion on Basal and Stimulated Nitric Oxide Activity in Neonatal Piglet Pulmonary Vessels

In vitro cell injury by oxidized low density lipoprotein involves lipid hydroperoxide-induced formation of alkoxyl, lipid, and peroxyl radicals.

Spectrophotometric Assay of Superoxide Anion Formed in Maillard Reaction Based on Highly Water-soluble Tetrazolium Salt

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