Analysis of cardiac membrane phospholipid peroxidation kinetics as malondialdehyde: Nonspecificity of thiobarbituric acid‐reactivity

Janero, David R.; Burghardt, Barbara

doi:10.1007/bf02535519

Cited by 86 publications

(36 citation statements)

References 41 publications

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“…We interpret these data to indicate that NOE inhibits MDA production by iron-induced lipid peroxidation primarily or only if the lipid substrate is the component of a membrane. It is also possible that free radical-induced peroxidation of cardiac mitochondria yields some nonlipid-derived TBA- reactive substances other than MDA, as was recently demonstrated with rat heart membranes [16]. Our present data do not indicate whether NOE acts as a free radical scavenger, stabilizes mitochondrial membranes against free radical attack, or inhibits the chain reaction leading to MDA.…”

Section: Resultscontrasting

confidence: 48%

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Effects of long‐chain N‐acylethanolamines on lipid peroxidation in cardiac mitochondria

Parinandi¹,

Schmid²

1988

FEBS Letters

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A long-chain N-acylethanolamine (N-oleoyl-2-aminoethanol) is shown to inhibit the production of thiobarbituric acidreactive substances in rat heart mitochondria treated with Fe?+ or Fe'+/ADP. The inhibition is concentration-dependent in the range X%150 PM of the agent and can be nearly complete depending on the type and amount of the free radicalgenerating system. Structural analogues of N-acylethanolamine are inhibitory as well, but neither oleic acid nor ethanolamine has measurable effects. N-Oleoyl-2-aminoethanol affects peroxidation of linoleic acid micelles only minimally and has no effect on deoxyribose peroxidation.N-Oleoyl-2-aminoethanol; Oxygen free radical; (Cardiac mitochondria)

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Section: Resultscontrasting

confidence: 48%

“…Because the TBA-reactivity assay is not specific for MDA, this method may also include certain other oxidation products [16].…”

Section: Methodsmentioning

confidence: 99%

Effects of long‐chain N‐acylethanolamines on lipid peroxidation in cardiac mitochondria

Parinandi¹,

Schmid²

1988

FEBS Letters

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“…The TBA reaction has frequently been used for measuring lipid peroxidation in biologic samples but has limitations because a part of the TBA-positive material does not originate from lipid peroxides. 29 Nevertheless, change in TBARS level remains a reliable index of lipid peroxidation, especially in comparative studies made on the same biologic material. In brain homogenates incubated under aerobic conditions, Rehncrona et ai 23 have shown that increases in TBARS level were correlated with the loss of polyunsaturated fatty acids.…”

Section: Discussionmentioning

confidence: 99%

Increased lipid peroxidation in vulnerable brain regions after transient forebrain ischemia in rats.

Bromont

Marie

Bralet

1989

Stroke

218

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We examined cerebral lipid peroxidation, estimated by a thiobarbituric acid test, in rat brain regions after 30 minutes of severe forebrain ischemia and at recirculation periods of up to 72 hours. The lipid peroxide levels remained unaltered in all brain regions during ischemia and during the first hour of recirculation but were selectively increased between 8 and 72 hours of recirculation in the ischemia-sensitive regions of the hippocampus, striatum, and cortex. The most pronounced increases (30-37%) were seen at 48 hours of recirculation. In contrast, lipid peroxide levels were unchanged in infarcted brain regions 24 hours after intracarotid injection of microspheres, indicating that reoxygenation of the ischemic brain is a prerequisite for lipid peroxidation. We assessed the lipid peroxidation capacity of cerebral homogenates obtained from rats subjected to ischemia and recirculation by measuring the production of lipid peroxides after aerobic incubation. The homogenates from rats exposed to 30 minutes of ischemia or to 1 hour of recirculation were not more susceptible to peroxidation. However, the production of lipid peroxides was selectively increased in the hippocampus, striatum, and cortex at 8-48 hours of recirculation, suggesting a loss of efficacy of the antioxidant systems. These results, showing a delayed and long-lasting increase in lipid peroxidation that occurs in ischemia-sensitive brain regions and parallels the development of neuronal necrosis, support the hypothesis that free radical processes participate in postischemic neuronal damage. (Stroke 1989;20:918-924) I t has been suggested that cellular damage in cerebral ischemia is at least partly due to oxidative damage, notably that caused by free radical formation and lipid peroxidation.1 However, definitive proof of its occurrence is still controversial. Several laboratories have provided evidence that lipid peroxidation occurs in vivo either during or after brain ischemia and reperfusion, 2 -8 but other data have failed to support the hypothesis.9 -12 The controversy derives from the different methods that have been used for the detection and analysis of lipid peroxidation or from the use of different models of brain ischemia.In our study, we investigated lipid peroxidation using the four-vessel occlusion model of transient ischemia, 13 which produces severe forebrain ischemia and leads to delayed neuronal necrosis in 17 Regional blood flow was therefore measured during and after vascular occlusion to record precisely the ischemic conditions. We assessed the extent of lipid peroxidation by measuring the level of thiobarbituric acidreactive substances (TBARS) in various cerebral structures at different times after the induction of ischemia. Simultaneously, we investigated the capacity of cerebral lipid peroxidation by measuring the accumulation of TBARS in brain homogenates incubated under aerobic conditions. Materials and MethodsWe performed the study with the four-vessel occlusion model on 98 male Wistar rats (Iffa Credo, France), wei...

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“…The concentration of thiobarbituric-acid-reactive substances (TBARS) was calculated using the absorption coefficient 1.56 X lo5 M-' cm-' [31]. This measurement may include TBARS arising from non-lipid sources [32].…”

Section: Determination Of Ca2+ Fluxesmentioning

confidence: 99%

Involvement of the ADP/ATP carrier in permeabilization processes of the inner mitochondrial membrane

Macedo

Nepomuceno

Pereira-Da-Silva

1993

European Journal of Biochemistry

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The effect of different agents on inner-mitochondrial-membrane permeabilization and lipoperoxidation induced by Ca2+ and the pyridine-nucleotide oxidant t-butylhydroperoxide or inorganic phosphate was investigated. Comparing the protection conferred by ADP, a substrate of the ADP/ATP carrier, dithiothreitol, a disulfide reductant and butylhydroxytoluene, a radical scavenger, it was found that ADP was always the most effective against mitochondrial damage, when present in the incubation medium from the beginning. Moreover, carboxyatractyloside, a specific inhibitor of the ADP/ATP carrier, abolished completely the protective effect of ADP on both the lipoperoxidation and mitochondrial swelling processes. Experiments where deenergized mitochondria were previously incubated with Ca2+ showed a decrease in the content of active ADP/ATP carrier, indicating a direct involvement of this protein in the formation of a non-specific Ca2+-dependent pore. Our results also eliminate the possibility of an attack of oxygen radicals on lipids or proteins of the mitochondrial membrane as the primary event triggering the permeability transition of the inner mitochondrial membrane.During the last two decades there have been several attempts to explain the mechanism of the Ca2+-induced permeabilization of the inner mitochondrial membrane when the organelle is loaded with Ca2+ in the presence of so called Ca2+-releasing agents [l -61. Organic hydroperoxides, diamide or inorganic phosphate (P,) have been used in most of these experiments, and different hypotheses arose to explain the observed permeabilization of mitochondria [l -61. More recently, the oxidation of either proteins [6] or phospholipids [5] of the inner mitochondrial membrane has been proposed as the molecular mechanism involved in these permeabilization processes. Supporting this suggestion, it was observed that both dithiotreitol and butylhydroxytoluene are able to protect the mitochondria against the deleterious effects of Ca2+ and either prooxidants or P, [5-81. In fact, this was only partially corroborated by our previous results, which showed the occurrence of lipoperoxidation when the mitochondria were incubated in the presence of Ca" and hydroperoxide, but not when the incubation was performed under conditions of high concentrations of Ca2+ and P, [9].Since the first evidence was presented that the Ca2+-induced permeabilization of mitochondria could be attributed to a reversible Ca2+-activated pore [lo], increasing amounts of data have been published supporting this hypothesis [ll-131. It was also shown that the removal of Ca2+ by the addition of EGTA was enough to reseal the mitochondrial mem- brane [lo, 111. The protein or proteins responsible for the pore opening and closure have not yet been identified, and a good candidate for such role is the ADP/ATP carrier. It is already known that both ADP and ATP and also the specific ADP/ATP-carrier inhibitor bongkrekate, are able to protect the mitochondrial membrane against the permeabilization processes [14-161. Ho...

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Analysis of cardiac membrane phospholipid peroxidation kinetics as malondialdehyde: Nonspecificity of thiobarbituric acid‐reactivity

Cited by 86 publications

References 41 publications

Effects of long‐chain N‐acylethanolamines on lipid peroxidation in cardiac mitochondria

Effects of long‐chain N‐acylethanolamines on lipid peroxidation in cardiac mitochondria

Increased lipid peroxidation in vulnerable brain regions after transient forebrain ischemia in rats.

Involvement of the ADP/ATP carrier in permeabilization processes of the inner mitochondrial membrane

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