Kinetik des Malondialdehydes im Organismus

Placer, Z; Veselková, A; Rath, R.

doi:10.1007/bf02136359

Cited by 37 publications

(7 citation statements)

References 3 publications

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“…MDA is formed distal to conjugated dienes and hydroperoxides, and the lack of an increase may reflect the alterations of hydroperoxides. MDA has been suggested to be an unsatisfactory indicator of lipid peroxidation in vivo (13,23) because MDA is readily metabolized in vivo and in tissue suspensions (24), partly by a mitochondrial aldehyde oxidase (25). It also reacts with tissue components to form cross-linked lipofuscin pigments, decreasing intracellular composition.…”

Section: Discussionmentioning

confidence: 99%

Oxygen Free Radical Effects in Sciatic Nerve in Experimental Diabetes

1991

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We previously reported the presence of endoneurial hypoxia, ischemia, impairment of the blood-nerve barrier, and reduction of norepinephrine and 6-ketoprostaglandin F1 alpha in chronic streptozocin-induced diabetic neuropathy (SDN) and interpreted these findings as suggesting the involvement of oxygen free radicals (OFRs) but did not directly measure indices of OFR activity. In this study, we report on sciatic nerve conjugated dienes, hydroperoxides, norepinephrine, and malondialdehyde in SDN at 1, 4, and 12 mo in male Sprague-Dawley rats. Severe hyperglycemia was present throughout in diabetic rats. Conjugated dienes were consistently increased at all time points, hydroperoxides were consistently reduced, and malondialdehyde was not significantly different in diabetes compared with controls. These findings are consistent with increased OFR activity in experimental diabetes. It is necessary to monitor several indices of OFR activity in a metabolically active tissue such as the peripheral nerve.

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Section: Discussionmentioning

confidence: 99%

Oxygen Free Radical Effects in Sciatic Nerve in Experimental Diabetes

1991

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“…Failure to detect TBA-rea c ting material in tissue extracts is not an indication of the absence of lipid peroxidation. Malonaldehyde, if injected, disappears within a few hours from the serum (11) and is metabolized by liver homogenates and fractions thereof (12,13). A second method for the detection of lipid peroxidation is to examine tissue extracts for the presence of conjugated dienes by ultraviolet spectrophotometry.…”

Section: Measurement Of Lipid Peroxida Nonmentioning

confidence: 99%

Chemicals, Drugs, and Lipid Peroxidation

Plaa¹,

Witschi²

1976

Annu. Rev. Pharmacol. Toxicol.

490

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“…Recknagel and Ghoshal (16) found that incubation of MA with rat liver homogenate or mitochondria led to disappearance of MA as measured by the thiobarbituric acid (TBA) assay. Placer et al (17) demonstrated the disappearance of TBA-reactive material in the tissues of rats injected intraperitoneally with MA. These observations may be attributed to oxidation of MA by the low specificity mitochondrial aldehyde dehydrogenase (18) and/or to reactions of MA with amino or sulfhydryl groups which can result in a decrease in TBA reactivity.…”

Section: Introductionmentioning

confidence: 99%

Metabolism of malonaldehyde in vivo and in vitro

SIu

Draper

1982

Lipids

179

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The metabolism of malonaldehyde (MA) was investigated in vivo using male Wistar rats and in vitro using rat liver mitochondria. Twelve hr after intubation with [1,3-14C] MA, 60-70%, 5-15% and 9-17% of administered radioactivity was recovered in expired CO2, feces and urine, respectively. In rats intubated with [1,2-14C) acetate, the corresponding values were 68-82%, 1-2% and 2.3%. 14CO2 evolution was initially slower after 14C-MA administration than after 14C-acetate administration and more radioactivity was excreted in the feces and urine. In vitro experiments using [1,3-14C] MA showed that MA is metabolized primarily in the mitochondria via reactions involving O2 utilization and 14CO2 production. The apparent Km and Vmax were 0.5 mM and 9.3 nmol/min/mg protein for O2 uptake, respectively, and 2.0 mM and 2.4 nmol/min/mg protein for 14CO2 production. Addition of malonic acid to mitochondrial incubates at concentrations inhibitory to succinate dehydrogenase did not affect MA-induced O2 uptake but enhanced 14CO2 production from 14C-MA. 14C-Acetate appeared to be the major accumulating metabolite in rat liver mitochondrial preparations following a 120-min incubation with 14C-MA. A probable biochemical route for MA metabolism involves oxidation of MA by mitochondrial aldehyde dehydrogenase followed by decarboxylation to produce CO2 and acetate.

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Kinetik des Malondialdehydes im Organismus

Cited by 37 publications

References 3 publications

Oxygen Free Radical Effects in Sciatic Nerve in Experimental Diabetes

Oxygen Free Radical Effects in Sciatic Nerve in Experimental Diabetes

Chemicals, Drugs, and Lipid Peroxidation

Metabolism of malonaldehyde in vivo and in vitro

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