Effect of acidosis on lipid peroxidation in brain slices

Bralet, J; Bouvier, Christine; Schreiber, Lisbeth; Boquillon, Micheline

doi:10.1016/0006-8993(91)90703-x

Cited by 63 publications

(20 citation statements)

References 15 publications

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“…Inhibition of the cytochrome c oxidase complex leads to anaerobic glycolysis and lactic acidosis-''histotoxic hypoxia'' (9). It was hypothesized that because of acidosis, the generation of oxygen radicals might be enhanced, leading to membrane damage, lipid peroxidation, and mitochondrial damage (10,11).…”

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confidence: 99%

An in vivo ESR spin-trapping study: Free radical generation in rats from formate intoxication— role of the Fenton reaction

Dikalova

Kadiiska

Mason

2001

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

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Electron spin resonance spectroscopy has been used to study free radical generation in rats with acute sodium formate poisoning. The in vivo spin-trapping technique was used with ␣-(4-pyridyl-1-oxide)-N-t-butylnitrone (POBN), which reacts with free radical metabolites to form radical adducts, which were detected in the bile and urine samples from Fischer rats. The use of [ 13 C]-sodium formate and computer simulations of the spectra identified the 12-line spectrum as arising from the POBN͞carbon dioxide anion radical adduct. The identification of POBN͞ ⅐ CO 2 ؊ radical adduct provides direct electron spin resonance spectroscopy evidence for the formation of ⅐ CO 2 ؊ radicals during acute intoxication by sodium formate, suggesting a free radical metabolic pathway. To study the mechanism of free radical generation by formate, we tested several known inhibitors. Both allopurinol, an inhibitor of xanthine oxidase, and aminobenzotriazole, a cytochrome P450 inhibitor, decreased free radical formation from formate, which may imply a dependence on hydrogen peroxide. In accord with this hypothesis, the catalase inhibitor 3-aminotriazole caused a significant increase in free radical formation. The iron chelator Desferal decreased the formation of free radicals up to 2-fold. Presumably, iron plays a role in the mechanism of free radical generation by formate via the Fenton reaction. The detection of formate free radical metabolites generated in vivo and the key role of the Fenton reaction in this process may be important for understanding the pathogenesis of both formate and methanol intoxication.

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confidence: 99%

An in vivo ESR spin-trapping study: Free radical generation in rats from formate intoxication— role of the Fenton reaction

Dikalova

Kadiiska

Mason

2001

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

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“…The most prominent assay currently being used as an index for lipid peroxidation in biological systems is the measurement of the thiobarbituric acid reactive substances (TBARS) through the thiobarbituric acid (TBA) test (Gutteridge and Halliwell, 1990). In the brain, this assay has been extensively used in the last three decades in several experimental models such as homogenates, synaptosomes, slices and in vivo, in an effort to elucidate the possible contribution of ROS to brain damage associated with several acute conditions such as hyperbaric oxygenation, brain ischemia, focal hemorrhage, traumatic brain injury and chronic disorders such as Huntington's chorea, Parkinson's and Alzheimer's diseases (Bawari et al, 1995;Boehme et al, 1977;Bralet et al, 1991;Chakraborty et al, 2001;Cini et al, 1994;Dirks and Faiman, 1982;Kücükkaya et al, 1996;Santamaría et al, 1999). This assay is based upon the formation of a red adduct (absorption maximum 532 nm) between TBA and malondialdehyde (MDA), a colorless end product of lipid peroxide decomposition (Janero, 1990).…”

Section: Introductionmentioning

confidence: 99%

Lipid peroxidation measurement by thiobarbituric acid assay in rat cerebellar slices

García

Rodrı́guez-Malaver

Peñaloza

2005

Journal of Neuroscience Methods

175

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“…7 Furthermore, acidosis increases TBARS in anoxic brain slices. 8 Although iron likely plays an important role in acidosis-mediated mechanisms of ischemic injury, the conditions of iron release, regional distribution of prooxidant iron, and participation in lipid peroxidation have not been clearly outlined.…”

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confidence: 99%

Low Molecular Weight Iron in Cerebral Ischemic Acidosis In Vivo

Lipscomb

Gorman

Traystman

et al. 1998

Stroke

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Background and Purpose-Iron-catalyzed radical generation is a potentially significant mechanism by which extensive tissue acidosis exacerbates brain injury during ischemia/reperfusion. We hypothesized that levels of low-molecular-weight (LMW) iron increase during in vivo global cerebral ischemia in a pH-dependent manner, potentially catalyzing oxidant injury. The present study quantified regional differences in LMW iron during global cerebral incomplete ischemia and determined whether augmenting the fall in ischemic tissue pH with hyperglycemia also amplifies free iron availability. Methods-Dogs anesthetized with pentobarbital-fentanyl were treated with 30 minutes of global incomplete cerebral ischemia produced by intracranial pressure elevation. Cerebral energy metabolites (ATP, phosphocreatine) and intracellular pH (pH i ) were measured by 31 P magnetic resonance spectroscopy. Preischemic plasma glucose level was manipulated to titrate end-ischemic pH i . After ischemia, brains were perfused with cold phosphate-buffered saline solution; then 16 different brain areas were sampled, filtered to separate the LMW fraction (Ͻ30 000 D), and assayed by rapid colorimetric assay for tissue iron. Total iron, LMW iron, and protein in each sample were measured in sham-operated (no ischemia, nϭ8), normoglycemic ischemia (ISCH [glucose 7Ϯ4 mmol/L], nϭ7), and hyperglycemic (GLU-ISCH [glucose 31Ϯ3 mmol/L], nϭ9) groups. Results-High-energy phosphates fell to near zero values in both ISCH and GLU-ISCH groups by 30 minutes but remained unchanged in the sham-operated group. As expected, pH i decreased during ischemia but to a greater extent in GLU-ISCH (6.20Ϯ0.05 in ISCH, 6.08Ϯ0.04 in GLU-ISCH, PϽ.05). Iron could be detected in all areas of the brain in sham-operated animals, with the highest amounts obtained from subcortical areas such as the hippocampus, pons, midbrain, and medulla. Total iron was higher in ISCH relative to sham-operated animals and higher in cortex and pons relative to GLU-ISCH. Regional LMW (as a percentage of total iron; LMW/total iron) was elevated in numerous brain areas in ISCH, including cortical gray matter, cerebellum, hippocampus, caudate, and midbrain. LMW/total iron was higher in GLU-ISCH versus ISCH in cortical gray matter only. In other brain areas, ischemic LMW/total iron was equivalent in glucose-treated or normoglycemic animals (white matter, thalamus, pons, medulla) or lower in the glucose-treated group (cerebellum, hippocampus, caudate, midbrain). Conclusions-These data demonstrate that levels of total and LMW iron increase with global cerebral ischemia in the majority of cortical and subcortical regions of normoglycemic brain. However, exacerbation of ischemic acidosis via glucose administration does not increase tissue iron and produces a greater increase in the LMW fraction in cortical gray matter only. In other brain regions, total and LMW iron availability is similar to that of nonischemic animals. (Stroke. 1998;29:487-493.)

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Effect of acidosis on lipid peroxidation in brain slices

Cited by 63 publications

References 15 publications

An in vivo ESR spin-trapping study: Free radical generation in rats from formate intoxication— role of the Fenton reaction

An in vivo ESR spin-trapping study: Free radical generation in rats from formate intoxication— role of the Fenton reaction

Lipid peroxidation measurement by thiobarbituric acid assay in rat cerebellar slices

Low Molecular Weight Iron in Cerebral Ischemic Acidosis In Vivo

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