Ferrous ion-EDTA-stimulated phospholipid peroxidation. A reaction changing from alkoxyl-radical- to hydroxyl-radical-dependent initiation

The stimulatory effect of ferrous salts on the peroxidation of phospholipids can be enhanced by EDTA when the concentration of Fe2+ in the reaction is greater than that of EDTA. Hydroxyl-radical scavengers do not inhibit peroxidation until the concentrations of Fe2+ and EDTA in the reaction are equal. Lipid peroxidation is then substantially initiated by hydroxyl radicals derived from a Fenton-type reaction requiring hydrogen peroxide. Superoxide radicals appear to play some role in the formation of initiating species.

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Gentamicin-induced mobilization of iron from renal cortical mitochondria

AJP Renal Physiology ◽

10.1152/ajprenal.1993.265.3.f435 ◽

1993 ◽

Vol 265 (3) ◽

pp. F435-F439 ◽

Cited By ~ 6

Author(s):

N. Ueda ◽

B. Guidet ◽

S. V. Shah

Keyword(s):

Hydrogen Peroxide ◽

Hydroxyl Radical ◽

Tissue Injury ◽

Iron Chelator ◽

Iron Release ◽

Radical Scavengers ◽

Iron Mobilization ◽

No Formation ◽

Hydroxyl Radical Scavengers ◽

Dose Dependent

Iron, presumably by participating in generation of hydroxyl radical or other oxidant species or initiation of lipid peroxidation, has been shown to play an important role in several models of tissue injury, including acute renal failure induced by the antibiotic gentamicin. However, the sources of iron remain unknown. Rat renal mitochondria incubated at 37 degrees C with gentamicin resulted in a time- (15-60 min) and a dose-dependent (0.01-5 mM) iron release as measured by formation of iron-bathophenanthroline sulfonate complex FeII-(BPS)3 [at 60 min, control: 1.2 +/- 0.1 nmol/mg protein, n = 7; gentamicin (5 mM): 5.1 +/- 0.4 nmol/mg protein, n = 7]. No formation of FeII(BPS)3 complex was detected in the absence of mitochondria or when incubations were carried out at 0 degrees C. Similar results were obtained when 2,2'-dipyridyl, another iron chelator, was used for measurement of iron release. On the basis on our previous study that gentamicin enhances generation of hydrogen peroxide by renal cortical mitochondria, we examined whether effect of gentamicin on iron release is mediated by hydrogen peroxide. Catalase (which decomposes hydrogen peroxide), but not heat-inactivated catalase, as well as pyruvate, a potent scavenger of hydrogen peroxide, prevented gentamicin-induced iron mobilization. Superoxide dismutase, a scavenger of superoxide anion, or hydroxyl radical scavengers (dimethylthiourea or sodium benzoate) had no effect. Taken together, the data with scavengers indicate that gentamicin-induced iron mobilization from mitochondria is mediated by hydrogen peroxide.

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Cytocidal and filamentous response ofEscherichia coli cells exposed to low concentrations of hydrogen peroxide and hydroxyl radical scavengers

Environmental and Molecular Mutagenesis ◽

10.1002/em.2850180105 ◽

1991 ◽

Vol 18 (1) ◽

pp. 22-27 ◽

Cited By ~ 9

Author(s):

Giorgio Brandi ◽

Leonardo Salvaggio ◽

Flaminio Cattabeni ◽

Orazio Cantoni ◽

K. E. Mortelmans

Keyword(s):

Hydrogen Peroxide ◽

Hydroxyl Radical ◽

Ofescherichia Coli ◽

Radical Scavengers ◽

Low Concentrations ◽

Hydroxyl Radical Scavengers

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Curculigo orchioides Protects Cisplatin-Induced Cell Damage

The American Journal of Chinese Medicine ◽

10.1142/s0192415x13500316 ◽

2013 ◽

Vol 41 (02) ◽

pp. 425-441 ◽

Cited By ~ 2

Author(s):

Tong Ho Kang ◽

Bin Na Hong ◽

Su-Young Jung ◽

Jeong-Han Lee ◽

Hong-Seob So ◽

...

Keyword(s):

Hydrogen Peroxide ◽

Lipid Peroxidation ◽

Hydroxyl Radicals ◽

Cell Damage ◽

Superoxide Radicals ◽

Ros Generation ◽

Protective Mechanism ◽

Dependent Manner ◽

Protective Effects ◽

Curculigo Orchioides

Cisplatin is commonly used as a chemotherapeutic agent against many human cancers. However, it generates reactive oxygen species (ROS) and has serious dose-limiting side effects, including ototoxicity. The roots of Curculigo orchioides (C. orchioides) have been used to treat auditory diseases such as tinnitus and hearing loss in Chinese traditional medicine. In the present study, we investigated the protective effects of an ethanol extract obtained from C. orchioides rhizome (COR) on cisplatin-induced cell damage in auditory cells (HEI-OC1). COR (2.5–25 μg/ml) inhibited cisplatin-induced HEI-OC1 cell damage in a dose-dependent manner. To investigate the protective mechanism of COR on cisplatin cytotoxicity in HEI-OC1 cells, we measured the effects of COR on ROS generation and lipid peroxidation in cisplatin-treated cells as well as its scavenging activities against superoxide radicals, hydroxyl radicals, hydrogen peroxide, and DPPH radicals. COR (1–25 μg/ml) had scavenging activities against superoxide radicals, hydroxyl radicals, hydrogen peroxide, and DPPH radicals, as well as reduced lipid peroxidation. In in vivo experiments, COR was shown to reduce cochlear and peripheral auditory function impairments through cisplatin-induced auditory damage in mice. These results indicate that COR protects from cisplatin-induced auditory damage by inhibiting lipid peroxidation and scavenging activities against free radicals.

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Inhibition of microsomal oxidation of alcohols and of hydroxyl-radical-scavenging agents by the iron-chelating agent desferrioxamine

Biochemical Journal ◽

10.1042/bj2100107 ◽

1983 ◽

Vol 210 (1) ◽

pp. 107-113 ◽

Cited By ~ 77

Author(s):

A I Cederbaum ◽

E Dicker

Keyword(s):

Hydroxyl Radical ◽

Hydroxyl Radicals ◽

Radical Scavenging ◽

Chelating Agent ◽

Dimethyl Sulphoxide ◽

The Other ◽

Radical Scavengers ◽

Primary Alcohols ◽

Hydroxyl Radical Scavengers ◽

Oxidation Of Ethanol

Rat liver microsomes (microsomal fractions) catalyse the oxidation of straight-chain aliphatic alcohols and of hydroxyl-radical-scavenging agents during NADPH-dependent electron transfer. The iron-chelating agent desferrioxamine, which blocks the generation of hydroxyl radicals in other systems, was found to inhibit the following microsomal reactions: production of formaldehyde from either dimethyl sulphoxide or 2-methylpropan-2-ol (t-butylalcohol); generation of ethylene from 4-oxothiomethylbutyric acid; release of 14CO2 from [I-14C]benzoate; production of acetaldehyde from ethanol or butanal (butyraldehyde) from butan-1-ol. Desferrioxamine also blocked the increase in the oxidation of all these substrates produced by the addition of iron-EDTA to the microsomes. Desferrioxamine had no effect on a typical mixed-function-oxidase activity, the N-demethylation of aminopyrine, nor on the peroxidatic activity of catalase/H2O2 with ethanol. H2O2 appears to be the precursor of the oxidizing radical responsible for the oxidation of the alcohols and the other hydroxyl-radical scavengers. Chelation of microsomal iron by desferrioxamine most likely decreases the generation of hydroxyl radicals, which results in an inhibition of the oxidation of the alcohols and the hydroxyl-radical scavengers. Whereas desferrioxamine inhibited the oxidation of 2-methylpropan-2-ol, dimethyl sulphoxide, 4-oxothiomethylbutyrate and benzoate by more than 90%, the oxidation of ethanol and butanol could not be decreased by more than 45-60%. Higher concentrations of desferrioxamine were required to block the metabolism of the primary alcohols than to inhibit the metabolism of the other substrates. The desferrioxamine-insensitive rate of oxidation of ethanol was not inhibited by competitive hydroxyl-radical scavengers. These results suggest that primary alcohols may be oxidized by two pathways in microsomes, one dependent on the interaction of the alcohols with hydroxyl radicals (desferrioxamine-sensitive), the other which appears to be independent of these radicals (desferrioxamine-insensitive).

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