Effect of intracellular iron loading on lipid peroxidation of brain slices

Oubidar, Mohamed; Boquillon, Micheline; Marie, Christine; Bouvier, Christine; Beley, A; Bralet, J

doi:10.1016/0891-5849(96)00173-6

Cited by 34 publications

(19 citation statements)

References 28 publications

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“…MDA: malondyaldehide; NOx: nitrates þ nitrites; MCD: methionine-choline deficient; LA: lipoic acid; Cx: cortex; H: hypothalamus; S: striatum; Hipp: hippocampus Veskovic et al LA affects the oxidative stress in brain in mice with methionine-choline deficiency 421 accumulation is of major concern, as the brain contains large quantities of iron and copper, which may catalyze the formation of hydroxyl radicals that can induce lipid peroxidation. 38 Enhanced hydrogen peroxide, in turn, is reduced to water by peroxidases, mostly GPx in the brain. 39 SOD catalyses the conversion of superoxide free radical to hydrogen peroxide and water, while GPx continues where SOD leaves off by catalyzing the reduction of hydrogen peroxide to water at the expense of glutathione.…”

Section: Discussionmentioning

confidence: 99%

Alpha-lipoic acid affects the oxidative stress in various brain structures in mice with methionine and choline deficiency

Vesković

Mladenović

Jorgačević

et al. 2014

Exp Biol Med (Maywood)

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Deficiency in methionine or choline can induce oxidative stress in various organs such as liver, kidney, heart, and brain. This study was to examine the effects of alpha-lipoic acid (LA) on oxidative stress induced by methionine and choline deficiency (MCD) in several brain structures. Male mice C57BL/6 (n ¼ 28) were divided into four groups: (1) control -continuously fed with standard chow; (2) LA -fed with standard chow and receiving LA; (3) MCD2 -fed with MCD diet for two weeks, and (4) MCD2þLA -fed with MCD diet for two weeks and receiving LA (100 mg/kg/day intraperitonealy [i.p.]). Brain tissue (cortex, hypothalamus, striatum and hippocampus) was taken for determination of oxidative stress parameters. MCD diet induced a significant increase in malondialdehyde and NOx concentration in all brain regions, while LA restored their content to normal values. Similar to this, in MCD2 group, activity of total SOD, MnSOD, and Cu/ZnSOD was reduced by MCD diet, while LA treatment improved their activities in all brain structures. Besides, in MCD2 group a decrease in catalase activity in cortex and GSH content in hypothalamus was evident, while LA treatment induced an increase in catalase activity in cortex and striatum and GSH content in hypothalamus. LA treatment can significantly reduce lipid peroxidation and nitrosative stress, caused by MCD diet, in all brain regions by restoring antioxidant enzymes activities, predominantly total SOD, MnSOD, and Cu/ZnSOD, and to a lesser extent by modulating catalase activity and GSH content. LA supplementation may be used in order to prevent brain oxidative injury induced by methionine and choline deficiency.

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Section: Discussionmentioning

confidence: 99%

Alpha-lipoic acid affects the oxidative stress in various brain structures in mice with methionine and choline deficiency

Vesković

Mladenović

Jorgačević

et al. 2014

Exp Biol Med (Maywood)

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“…Iron plays important roles in metabolic processes of animals, however, in toxic amounts may stimulate the production of free radicals by different mechanisms. Participate in Fenton-type reactions producing OH • radical (Fraga and Oteiza, 2002); may form complexes with oxygen as the complex Fe 2+ -O 2 -Fe 3+ , which are responsible for initiating lipid peroxidation reactions (Oubidar et al, 1996); degrade lipid hydroperoxide (ROOH) forming alkoxyl radical (RO • ) (Lima and Abdalla, 2001). Thus, the antioxidant activity of the extracts involving the prevention of lipid peroxidation and deoxyribose degradation by OH • radical can correlates with its iron chelating properties.…”

Section: Iron Chelation Assaymentioning

confidence: 99%

Phytochemical analysis and antioxidant activities of Lantana camara and Lantana montevidensis extracts

Sousa

Miranda

Nobre

et al. 2015

Industrial Crops and Products

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“…However, it can stimulate free radical production by different mechanisms (38,39): (a) via the breakdown of preexisting lipid hydroperoxides (ROOH) present in tissues forming lipid alkoxyl radical (RO • ); (b) by entering a Fenton type reaction producing hydroxyl radical; or (c) via formation of iron oxygen complexes such as perferryl ions or ferrous-dioxygen-ferric complexes, which initiates lipid peroxidation (18,40).…”

Section: Introductionmentioning

confidence: 99%

Krebs Cycle Intermediates Modulate Thiobarbituric Acid Reactive Species (TBARS) Production in Rat Brain In Vitro

2005

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The aim of this study was to investigate the effect of Krebs cycle intermediates on basal and quinolinic acid (QA)- or iron-induced TBARS production in brain membranes. Oxaloacetate, citrate, succinate and malate reduced significantly the basal and QA-induced TBARS production. The potency for basal TBARS inhibition was in the order (IC50 is given in parenthesis as mM) citrate (0.37) > oxaloacetate (1.33) = succinate (1.91) > > malate (12.74). alpha-Ketoglutarate caused an increase in TBARS production without modifying the QA-induced TBARS production. Cyanide (CN-) did not modify the basal or QA-induced TBARS production; however, CN- abolished the antioxidant effects of succinate. QA-induced TBARS production was enhanced by iron ions, and abolished by desferrioxamine (DFO). The intermediates used in this study, except for alpha-ketoglutarate, prevented iron-induced TBARS production. Oxaloacetate, citrate, alpha-ketoglutarate and malate, but no succinate and QA, exhibited significantly iron-chelating properties. Only alpha-ketoglutarate and oxaloacetate protected against hydrogen peroxide-induced deoxyribose degradation, while succinate and malate showed a modest effect against Fe2+/H2O2-induced deoxyribose degradation. Using heat-treated preparations citrate, malate and oxaloacetate protected against basal or QA-induced TBARS production, whereas alpha-ketoglutarate induced TBARS production. Succinate did not offer protection against basal or QA-induced TBARS production. These results suggest that oxaloacetate, malate, succinate, and citrate are effective antioxidants against basal and iron or QA-induced TBARS production, while alpha-ketoglutarate stimulates TBARS production. The mechanism through which Krebs cycle intermediates offer protection against TBARS production is distinct depending on the intermediate used. Thus, under pathological conditions such as ischemia, where citrate concentrations vary it can assume an important role as a modulator of oxidative stress associated with such situations.

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Effect of intracellular iron loading on lipid peroxidation of brain slices

Cited by 34 publications

References 28 publications

Alpha-lipoic acid affects the oxidative stress in various brain structures in mice with methionine and choline deficiency

Alpha-lipoic acid affects the oxidative stress in various brain structures in mice with methionine and choline deficiency

Phytochemical analysis and antioxidant activities of Lantana camara and Lantana montevidensis extracts

Krebs Cycle Intermediates Modulate Thiobarbituric Acid Reactive Species (TBARS) Production in Rat Brain In Vitro

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