Reactions of 1-Methyl-2-phenylindole with Malondialdehyde and 4-Hydroxyalkenals. Analytical Applications to a Colorimetric Assay of Lipid Peroxidation

Gérard-Monnier, Dominique; Erdelmeier, Irène; Régnard, Kheira; Moze-Henry, Nathalie; Yadan, Jean‐Claude; Chaudière, Jean

doi:10.1021/tx9701790

Cited by 418 publications

(239 citation statements)

References 36 publications

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“…Lipid peroxidation was detected measuring the intracellular level of malonyldialdehyde (MDA), the end product derived from the breakdown of polyunsaturated fatty acids and related esters (25), with the lipid peroxidation assay kit (Oxford Biomedical Research, Oxford, MI), which uses the reaction of N-methyl-2-phenylindole with MDA in the presence of hydrochloric acid to yield a stable chromophore with maximal absorbance at 586 nm (26).…”

Section: Methodsmentioning

confidence: 99%

Diphenyleneiodonium Inhibits the Cell Redox Metabolism and Induces Oxidative Stress

Riganti

Gazzano

Polimeni

et al. 2004

Journal of Biological Chemistry

179

133

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Diphenyleneiodonium (DPI) and the structurally related compound diphenyliodonium (DIP) are widely used as inhibitors of flavoenzymes, particularly NADPH oxidase. Here we report further evidence that DPI and DIP are not specific flavin binders. A 3-h incubation of N11 glial cells with DPI significantly inhibited in a dosedependent way both the pentose phosphate pathway and the tricarboxylic acid cycle. In parallel, we observed a dose-dependent increase of reactive oxygen species generation and lipoperoxidation and increased leakage of lactate dehydrogenase activity in the extracellular medium. The glutathione/glutathione disulfide ratio decreased, whereas the efflux of glutathione out of the cells increased. This suggests that DPI causes an augmented oxidative stress and exerts a cytotoxic effect in N11 cells. Indeed, the cells were protected from these events when loaded with glutathione. Similar results were observed using DIP instead of DPI and also in other cell types. We suggest that the DPI-elicited inhibition of the pentose phosphate pathway and tricarboxylic acid cycle may be mediated by the blockade of several NAD(P)-dependent enzymes, such as glucose 6-phosphate dehydrogenase, glyceraldehyde 3-phosphate dehydrogenase, and lactate dehydrogenase. In light of these results, we think that some effects of DPI or DIP in in vitro and in vivo experimental models should be interpreted with caution. Diphenyleneiodonium (DPI) 1 and the structurally related compound diphenyliodonium (DIP) are widely used as uncompetitive inhibitors of flavoenzymes. Firstly identified as a hypoglycemic agent able to block gluconeogenesis and respiration in rat liver (1), DPI has been subsequently shown to inhibit the activity of NADH:ubiquinone oxidoreductase (2, 3), NADPH oxidase (4 -6), nitric-oxide synthase (7), xanthine oxidase (6), and NADPH cytochrome P450 oxidoreductase (8). DPI and other iodonium derivatives have been shown to react via a radical mechanism, whereby an electron is abstracted from FAD or FMN to form a radical, which then adds back to the flavin to form covalent, phenylated adducts (9). Also, heme groups, such as the heme b of NADPH oxidase, have been found to react with DPI and DIP (10).In most experimental works of the last years, DPI or DIP have been used as inhibitors of NADPH oxidase. NADPH oxidases are a group of plasma membrane-associated enzymes found in a variety of cells of mesodermal origin. The most thoroughly studied is the leukocyte isoform, which catalyzes the production of superoxide (O 2 . ) by the one-electron reduction of oxygen, using NADPH as the reducing agent (11). The O 2 .generated by NADPH oxidase serves as the starting material for the production of a vast assortment of reactive oxidants used by phagocytes to kill invading microorganisms or tumor cells (11). A low activity NADPH oxidase is present in a variety of nonphagocytic cells, wherein this enzyme is a source of second messengers. It has been postulated, for instance, that the O 2 . generated by the aorta functions as a blood ...

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Section: Methodsmentioning

confidence: 99%

Diphenyleneiodonium Inhibits the Cell Redox Metabolism and Induces Oxidative Stress

Riganti

Gazzano

Polimeni

et al. 2004

Journal of Biological Chemistry

179

133

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“…The lipid peroxidation productions, HNE and malondialdehyde, were measured according to ref. 46 with tissue prepared by grinding rosette leaves to fine powder under liquid N 2 and adding 1:2.97 (g fresh weight/ml) 20 mM Tris (HCL) (pH 7.4), and 30 l of 500 mM butylated hydroxytoluene/g fresh weight.…”

Section: Insertional Mutantmentioning

confidence: 99%

Mitochondrial uncoupling protein is required for efficient photosynthesis

Sweetlove

Lytovchenko

Morgan

et al. 2006

Proc. Natl. Acad. Sci. U.S.A.

229

203

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Uncoupling proteins (UCPs) occur in the inner mitochondrial membrane and dissipate the proton gradient across this membrane that is normally used for ATP synthesis. Although the catalytic function and regulation of plant UCPs have been described, the physiological purpose of UCP in plants has not been established. Here, biochemical and physiological analyses of an insertional knockout of one of the Arabidopsis UCP genes (AtUCP1) are presented that resolve this issue. Absence of UCP1 results in localized oxidative stress but does not impair the ability of the plant to withstand a wide range of abiotic stresses. However, absence of UCP1 results in a photosynthetic phenotype. Specifically there is a restriction in photorespiration with a decrease in the rate of oxidation of photorespiratory glycine in the mitochondrion. This change leads to an associated reduced photosynthetic carbon assimilation rate. Collectively, these results suggest that the main physiological role of UCP1 in Arabidopsis leaves is related to maintaining the redox poise of the mitochondrial electron transport chain to facilitate photosynthetic metabolism. mitochondria ͉ Arabidopsis ͉ electron transport ͉ reactive oxygen species ͉ photorespiration

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“…The levels of MDA were determined spectrophotometrically by following a modified protocol developed by Gerard-Monnier et al (1998). This procedure measures free MDA as opposed to the commonly used TBARS (thiobarbituric acid-reactive substances) method which measures total MDA in biological samples.…”

Section: Malondialdehyde (Mda) Assaymentioning

confidence: 99%

Aluminum and copper in drinking water enhance inflammatory or oxidative events specifically in the brain

Becaria

Lahiri

Bondy

et al. 2006

Journal of Neuroimmunology

120

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Inflammatory and oxidative events are up-regulated in the brain of AD patients. It has been reported that in animal models of AD, exposure to aluminum (Al) or copper (Cu) enhanced oxidative events and accumulation of amyloid beta (Ah) peptides. The present study was designed to evaluate the effect of a 3-month exposure of mice to copper sulfate (8 AM), aluminum lactate (10 or 100 AM), or a combination of the salts. Results suggest that although Al or Cu may independently initiate inflammatory or oxidative events, they may function cooperatively to increase APP levels. D

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Reactions of 1-Methyl-2-phenylindole with Malondialdehyde and 4-Hydroxyalkenals. Analytical Applications to a Colorimetric Assay of Lipid Peroxidation

Cited by 418 publications

References 36 publications

Diphenyleneiodonium Inhibits the Cell Redox Metabolism and Induces Oxidative Stress

Diphenyleneiodonium Inhibits the Cell Redox Metabolism and Induces Oxidative Stress

Mitochondrial uncoupling protein is required for efficient photosynthesis

Aluminum and copper in drinking water enhance inflammatory or oxidative events specifically in the brain

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