Iron-initiated tissue oxidation: Lipid peroxidation, vitamin e destruction and protein thiol oxidation

Kl, Linseman; Larson, P G; Jm, Braughler; Jm, McCall

doi:10.1016/0006-2952(93)90048-2

Cited by 22 publications

(4 citation statements)

References 12 publications

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“…Vitamin E is one of the major lipid-soluble chain-breaking antioxidants in biological systems [26] that incorporate into the plasma membrane. It acts by interfering with the propagation of lipid peroxidation chain reaction [55], by scavenging lipid peroxyl and alkoxyl radicals [56]. Idebenone is a structural analog of ubiquinone [29], which has been suggested to act as an electron carrier, like ubiquinone and also as a free radical scavenger.…”

Section: Discussionmentioning

confidence: 99%

Mitochondrial function is differentially affected upon oxidative stress

Cardoso

Pereira

Oliveira

1999

Free Radical Biology and Medicine

121

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Abstract-The mechanisms that lead to mitochondrial damage under oxidative stress conditions were examined in synaptosomes treated with ascorbate/iron. A loss of membrane integrity, evaluated by electron microscopy and by LDH leakage, was observed in peroxidized synaptosomes and it was prevented by pre-incubation with vitamin E (150 M) and idebenone (50 M). ATP levels decreased, in synaptosomes exposed to ascorbate/iron, as compared to controls. NADH-ubiquinone oxidoreductase (Cx I) and cytochrome c oxidase (Cx IV) activities were unchanged after ascorbate/ iron treatment, whereas succinate-ubiquinone oxidoreductase (Cx II), ubiquinol cytochrome c reductase (Cx III) and ATP-synthase (Cx V) activities were reduced by 55%, 40%, and 55%, respectively. The decrease of complex II and ATP-synthase activities was prevented by reduced glutathione (GSH), whereas the other antioxidants tested (vitamin E and idebenone) were ineffective. However, vitamin E, idebenone and GSH prevented the reduction of complex III activity observed in synaptosomes treated with ascorbate/iron. GSH protective effect suggests that the oxidation of protein SH-groups is involved in the inhibition of complexes II, III and V activity, whereas vitamin E and idebenone protection suggests that membrane lipid peroxidation is also involved in the reduction of complex III activity. These results may indicate that the inhibition of the mitochondrial respiratory chain enzymatic complexes, that are differentially affected by oxidative stress, can be recovered by specific antioxidants.

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Section: Discussionmentioning

confidence: 99%

Mitochondrial function is differentially affected upon oxidative stress

Cardoso

Pereira

Oliveira

1999

Free Radical Biology and Medicine

121

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“…The above reactions lead to the production of the free hydroxyl radical, which is very short-lived because of its high reactivity, which leads to lipid peroxidation and protein and nucleic acid damage. Whether the free hydroxyl radical or the similarly reactive ferryl radical is produced by the Fenton reaction, as some authors suggest, 64,65 the results are damaging for the cell. The Figure shows a simplified model of the abnormalities of iron and free radical metabolism that may be induced by frataxin deficiency.…”

Section: Relevance For the Pathogenesis Of The Human Diseasementioning

confidence: 99%

“…In addition to the scavenging action of SOD2 and glutathione peroxidase, a front-line defense against free hydroxyl radical-induced lipid peroxidation is offered by vitamin E, 70% of which is localized in the inner mitochondrial membrane. 65 Interestingly, vitamin E deficiency causes an FRDA-like disease. 66…”

Section: Relevance For the Pathogenesis Of The Human Diseasementioning

confidence: 99%

Molecular Pathogenesis of Friedreich Ataxia

Pandolfo¹

1999

Arch Neurol

104

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Friedreich ataxia, the most common type of inherited ataxia, is itself caused in most cases by a large expansion of an intronic GAA repeat, resulting in decreased expression of the target frataxin gene. The autosomal recessive inheritance of the disease gives this triplet repeat mutation some unique features of natural history and evolution. Frataxin is a mitochondrial protein that has homologues in yeast and even in gram-negative bacteria. Yeast organisms deficient in the frataxin homologue accumulate iron in mitochondria and show increased sensitivity to oxidative stress. This suggests that Friedreich ataxia is caused by mitochondrial dysfunction and free radical toxicity.

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“…Sensitization of the rats 0007-4888/94/0006-0622512.50 @1994 Plenum Publishing Corporation was induced by i.p. For the study of the effect of the drug on the level of LPO in FeSO 4 induction the latter was caused by introducing 200 gM FeSO 4 into a test tube after the addition of the appropriate amount of drug to the incubation mixture [15]. The model of bronchospasm was performed by having preliminarily sensitized rats inhale an effective dose of egg albumin 4 h prior to the experiment.…”

Section: Methodsmentioning

confidence: 99%

The development of free radical processes in experimental bronchospasm. Effect of the bronchodilator preparation troventol

et al. 1994

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The development of bronchospasm is shown to be accompanied by hpid peroxidation (LPO) activation; 3-fold and 8-fold rises of malondialdehyde concentration are found in homogenate of lung from sensitized animals and from animals provoked with egg albumin antigen, respectively. The use of luminol-dependent chemiluminescence (CL) reveals that in sensitized rats the production of oxygen free radicals is increased by alveolar macrophages activated with phorbol myristate acetate. Troventol at 10 -3 mg/rnl inhibits the CL response of phagocytes both in intact and in sensitized rats and lowers the level of Fe2+-induced LPO in lung tissue but not in the liver of intact animals.

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Iron-initiated tissue oxidation: Lipid peroxidation, vitamin e destruction and protein thiol oxidation

Cited by 22 publications

References 12 publications

Mitochondrial function is differentially affected upon oxidative stress

Mitochondrial function is differentially affected upon oxidative stress

Molecular Pathogenesis of Friedreich Ataxia

The development of free radical processes in experimental bronchospasm. Effect of the bronchodilator preparation troventol

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