Formation of reactive aldehydes from fatty acids in a iron(2+)/hydrogen peroxide oxidation system

Tamura, Hirotoshi; Kitta, Kazumi; Shibamoto, Takayuki

doi:10.1021/jf00003a002

Cited by 80 publications

(52 citation statements)

References 11 publications

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“…In this paper, we present evidence that quercetin and genistein can inhibit Fe-and Cu-induced oxidative damage in U937 cells. It has been proposed that in the presence of H 2 O 2 these metal ions generate hydroxyl radical-like species through Fenton-type reactions, which may result in the degradation of proteins and nucleic acids or the peroxidative decomposition of polyunsaturated fatty acid (PUFA) (Tamura et al, 1991;Stinson et al, 1992;Minotti 1993;Kennedy et al, 1997). Experimental reagents such as Fe, Cu and H 2 O 2 , which can affect the formation of lipid peroxides as measured by the TBA assay (Duthie et al, 1997), were tested prior to the analysis of lipid peroxides.…”

Section: Discussionmentioning

confidence: 99%

In vitro exposure to quercetin and genistein alters lipid peroxides and prevents the loss of glutathione in human progenitor mononuclear (U937) cells

Boadi

Iyere

Adunyah

2005

J of Applied Toxicology

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The effects of flavonoids quercetin and genistein were investigated according to their potency to inhibit the oxidation of U937 cells via Fenton's pathway through the analysis of lipid peroxides and glutathione (GSH) levels. Human leukemia (U937) cells from the American Type Culture Collection were maintained at 37 degrees C for 24 h under 5% CO2 tension in RPMI-1640 medium containing 10% fetal bovine serum and 50 units ml(-1) each of penicillin and streptomycin. Cells were oxidized with iron 50 microM) or copper (50 microM) in H2O2 (0.01 mM) without or with a flavonoid sample (10 or 20 microM) for the lipid peroxidation studies. The GSH levels were measured (GSH Kit) before and after oxidation as above with different concentrations of flavonoids (0-40 microM). Lipid peroxide was measured by the thiobarbituric acid assay. Both quercetin and genistein at either the 10 or 20 microM level decreased lipid peroxidation significantly compared with their respective controls (P < 0.01). Lipid peroxides by Fe compared to the Cu-treated samples did not differ significantly from each other. However, the combination of flavonoids at the doses tested significantly (P < 0.001) decreased lipid peroxides, the effect being the same for both metal ions. The GSH levels increased significantly before exposure to the metal ions (for the different doses for the differences between the flavonoid samples and their respective untreated levels). For quercetin and genistein the increases in GSH above their untreated levels were 4.5, 8.3, 11.7 and 15 and 3.8, 7.9, 12.5 and 14.6 nmol 10(-6) cells, respectively, for the 5-40 microM levels tested for each flavonoid. Following the exposure to the metal ions, GSH levels remained almost the same for the different concentrations for each of the flavonoids tested but significantly above all of the controls and same for those of the untreated samples. The results indicate that both flavonoids inhibited lipid peroxides and the inhibition may be attributed to the prevention of loss of intracellular GSH levels in U937 cells.

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Section: Discussionmentioning

confidence: 99%

In vitro exposure to quercetin and genistein alters lipid peroxides and prevents the loss of glutathione in human progenitor mononuclear (U937) cells

Boadi

Iyere

Adunyah

2005

J of Applied Toxicology

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“…Small amounts of acrolein were detected upon Fe 2+ /H 2 O 2 -mediated oxidation of PUFAs and their ethyl esters (0.8-13 nmol/mg), but no detectable amounts of acrolein were generated from the mono-unsaturated fatty acid, oleic acid, or its ethyl ester [21]. A detailed and thorough study conducted by Pan and co-workers [22] indicates that acrolein can be released from the ethyl ester of the n-3 PUFA, all-cis-7,10,13,16,19-docosapentaenoic acid, by autoxidation at 50°C.…”

Section: Lipids As a Source Of Acroleinmentioning

confidence: 99%

Acrolein: Sources, metabolism, and biomolecular interactions relevant to human health and disease

Stevens

Maier

2008

Molecular Nutrition Food Res

633

634

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Acrolein (2-propenal) is ubiquitously present in (cooked) foods and in the environment. It is formed from carbohydrates, vegetable oils and animal fats, amino acids during heating of foods, and by combustion of petroleum fuels and biodiesel. Chemical reactions responsible for release of acrolein include heat-induced dehydration of glycerol, retro-aldol cleavage of dehydrated carbohydrates, lipid peroxidation of polyunsaturated fatty acids, and Strecker degradation of methionine and threonine. Smoking of tobacco products equals or exceeds the total human exposure to acrolein from all other sources. The main endogenous sources of acrolein are myeloperoxidase-mediated degradation of threonine and amine oxidase-mediated degradation of spermine and spermidine, which may constitute a significant source of acrolein in situations of oxidative stress and inflammation. Acrolein is metabolized by conjugation with glutathione and excreted in the urine as mercapturic acid metabolites. Acrolein forms Michael adducts with ascorbic acid in vitro, but the biological relevance of this reaction is not clear. The biological effects of acrolein are a consequence of its reactivity towards biological nucleophiles such as guanine in DNA and cysteine, lysine, histidine, and arginine residues in critical regions of nuclear factors, proteases, and other proteins. Acrolein adduction disrupts the function of these biomacromolecules which may result in mutations, altered gene transcription, and modulation of apoptosis.

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“…58 Blood samples may be kept at 4-5 ºC until centri fugation 49,50 to prevent transformation of MDA in other compound or its reaction with other cellular components, resulting in erroneous results.…”

Section: Sample Preparation and Storagementioning

confidence: 99%

Importance of the lipid peroxidation biomarkers and methodological aspects FOR malondialdehyde quantification

Grotto¹,

Maria²,

Valentini³

et al. 2009

Quím. Nova

356

251

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Recebido em 16/2/07; aceito em 7/3/08; publicado na web em 31/10/08Free radicals induce lipid peroxidation, playing an important role in patho logical processes. The injury mediated by free radicals can be measured by conjugated dienes, malon dial dehyde, 4-hydroxynonenal, and others. However, malondialdehyde has been pointed out as the main product to evaluate lipid peroxidation. Most assays determine malondialdehyde by its reaction with thiobarbituric acid, which can be mea sured by indirect (spectrometry) and direct methodologies (chromatography). Though there is some controversy among the methodologies, the selective HPLC-based assays provide a more reliable lipid peroxidation measure. This review describes significant aspects about MDA deter mination, its importance in pathologies and biological samples treatment.

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Formation of reactive aldehydes from fatty acids in a iron(2+)/hydrogen peroxide oxidation system

Cited by 80 publications

References 11 publications

In vitro exposure to quercetin and genistein alters lipid peroxides and prevents the loss of glutathione in human progenitor mononuclear (U937) cells

In vitro exposure to quercetin and genistein alters lipid peroxides and prevents the loss of glutathione in human progenitor mononuclear (U937) cells

Acrolein: Sources, metabolism, and biomolecular interactions relevant to human health and disease

Importance of the lipid peroxidation biomarkers and methodological aspects FOR malondialdehyde quantification

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