Visible chemiluminescence from rat brain homogenates undergoing autoxidation. I. Effect of additives and products accumulation

Lissi, E. A.; Cáceres, T.; Videla, Luis A.

doi:10.1016/0748-5514(86)90125-x

Cited by 46 publications

(17 citation statements)

References 19 publications

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“…[33][34][35][36][37] The use of tissue homogenate offered several advantages: it was easier to obtain relatively large amounts of fresh material; for initial processing under simple standard conditions, no extraneous catalyst was required; the rate and pattern of spontaneous autoxidation was remarkably regular, precise and reproducible. 27,33,38 A good parameter to compare the antioxidant activity of the various compounds was the concentration inhibiting 50% (IC 50 ) of brain homogenate autoxidation, that is to say that lower IC 50 values corresponded to higher antioxidant activities. The IC 50 values were calculated by a statistical model, with a specific polynomial equation, of dose (concentration of antioxidants (μM)) as a function of effect (antioxidant activity (%)).…”

Section: Determining Antiradical and Antioxidant Capacitiesmentioning

confidence: 99%

The synthesis of a water-soluble derivative of rutin as an antiradical agent

Pedriali¹,

Fernandes²,

Bernusso³

et al. 2008

Quím. Nova

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Recebido em 13/6/07; aceito em 20/6/08; publicado na web em 31/10/08The purpose of this study was to synthesize a water-soluble derivative of rutin (compound 2) by introducing carboxylate groups on rutin's sugar moiety. The rutin derivative showed an almost 100-fold solubility increase in water. The antiradical capacity of compound 2 was evaluated using the luminol/AAPH system, and the derivative's activity was 1.5 times greater than that of Trolox ® . Despite the derivative's high solubility in water (log P = -1.13), lipid peroxidation of brain homogenate membranes was very efficiently inhibited (inhibition values were only 19% lower than the inhibition values of rutin).

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Section: Determining Antiradical and Antioxidant Capacitiesmentioning

confidence: 99%

The synthesis of a water-soluble derivative of rutin as an antiradical agent

Pedriali¹,

Fernandes²,

Bernusso³

et al. 2008

Quím. Nova

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“…The steady increase in chemiluminescence is compatible with that expected if the emission arises from the decomposition of an oxidation product. 19,26,29 Furthermore, it is interesting to note that this emission is higher than that observed in the oxidation of histidine (Table 1), indicating that the conjugated double bond in urocanic acid contributes to the formation of chemiluminescence precursors. In order to have some insight on the mechanism of the chemiluminescence and the characteristics of its precursor, we added Ebselen (a compound with peroxidase-like activity) and Trolox (an efficient free radical scavenger) after 270 min incubation.…”

Section: Consumption Of Urocanic Acid Mediated By Peroxyl Radicalsmentioning

confidence: 85%

“…This phenomenon is observed in the oxidation of cells, tissues and organs. [25][26][27][28] Products generated in the interaction of trans-urocanic acid with peroxyl radicals also emit a weak chemiluminescence. A typical profile, obtained when trans-urocanic acid is incubated with AAPH is shown in Figure 3A.…”

Section: Consumption Of Urocanic Acid Mediated By Peroxyl Radicalsmentioning

confidence: 99%

“…The chemiluminescence quenching by Ebselen would suggest that the emission precursor is a peroxide-like compound, while the almost total quenching elicited by Trolox addition would indicate that the chemiluminescence process is promoted by free radicals. 19,[26][27][28] It is interesting to note that, as in more complex systems, 29 chemiluminescence is strongly enhanced when the temperature increases. Typical data obtained when the sample preincubated at 37°C is introduced into the scintillation counter (kept at 23°C) are shown in Figure 3B.…”

Section: Consumption Of Urocanic Acid Mediated By Peroxyl Radicalsmentioning

confidence: 99%

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Interaction and reactivity of urocanic acid towards peroxyl radicals

et al. 2005

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The capacity of urocanic acid to interact with peroxyl radicals has been evaluated in several systems: oxidation in the presence of a free radical source (2,2'-azobis(2-amidinopropane; AAPH), protection of phycocyanin bleaching elicited by peroxyl radicals, and Cu(II)- and AAPH-promoted LDL oxidation. The results indicate that both isomers (cis and trans) are mild peroxyl radical scavengers. For example, trans-urocanic acid is nearly 400 times less efficient than Trolox in the protection of the peroxyl radical promoted bleaching of phycocyanin. Regarding the removal of urocanic acid by peroxyl radicals, nearly 100 muM trans-urocanic acid is required to trap half of the produced radicals under the employed conditions (10 mM AAPH, 37 degrees C). Competitive experiments show that the cis-isomer traps peroxyl radicals 30% less efficiently than the trans-isomer. Given the high concentrations that trans-urocanic acid reaches in skin, its capacity to trap peroxyl radicals could contribute to the protection of the tissue towards ROS-mediated processes. Furthermore, both isomers, and particularly the cis-isomer, protect LDL from Cu(II)-induced oxidation.

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“…Cerebral cortex was homogenized in 10 volumes (1:10, w/v) of 20 mM sodium phosphate buffer, pH 7.4 containing 140 mM KCl. Homogenates were centrifuged at 750 × g for 10 min at 4 °C to discard nuclei and cell debris (Llesuy et al, 1985; Lissi et al, 1986). The pellet was discarded and the supernatant was immediately separated and used for the measurements.…”

Section: Methodsmentioning

confidence: 99%

N‐Acetylaspartic acid promotes oxidative stress in cerebral cortex of rats

Pederzolli

Mescka

Scapin

et al. 2007

Intl J of Devlp Neuroscience

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N-acetylaspartic acid accumulates in Canavan Disease, a severe leukodystrophy characterized by swelling and spongy degeneration of the white matter of the brain. This inherited metabolic disease, caused by deficiency of the enzyme aspartoacylase, is clinically characterized by severe mental retardation, hypotonia and macrocephaly, and also generalized tonic and clonic type seizures in about half of the patients. Considering that the mechanisms of brain damage in this disease remain not fully understood, in the present study we investigated whether oxidative stress is elicited by N-acetylaspartic acid. The in vitro effect of N-acetylaspartic acid (10-80 mM) was studied on oxidative stress parameters: total radical-trapping antioxidant potential (TRAP), total antioxidant reactivity (TAR), chemiluminescence, thiobarbituric acid-reactive substances (TBA-RS), reduced glutathione content, sufhydryl content and carbonyl content in the cerebral cortex of 14-day-old rats. The effect of the acute administration of N-acetylaspartic acid (0.1-0.6 mmol/g body weight) was studied on TRAP, TAR, carbonyl content, chemiluminescence and TBA-RS. TRAP, TAR, reduced glutathione content and sulfhydryl content were significantly reduced, while chemiluminescence, TBA-RS and carbonyl content were significantly enhanced by N-acetylaspartic acid in vitro. The enhancement in TBA-RS promoted by N-acetylaspartic acid was completely prevented by ascorbic acid plus Trolox, and partially prevented by glutathione and dithiothreitol. The acute administration of N-acetylaspartic acid also significantly reduced TRAP and TAR, and significantly enhanced carbonyl content, chemiluminescence and TBA-RS. Our results indicate that N-acetylaspartic acid promotes oxidative stress by stimulating lipid peroxidation, protein oxidation and by decreasing non-enzymatic antioxidant defenses in rat brain. This could be another pathophysiological mechanism involved in Canavan Disease.

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Visible chemiluminescence from rat brain homogenates undergoing autoxidation. I. Effect of additives and products accumulation

Cited by 46 publications

References 19 publications

The synthesis of a water-soluble derivative of rutin as an antiradical agent

The synthesis of a water-soluble derivative of rutin as an antiradical agent

Interaction and reactivity of urocanic acid towards peroxyl radicals

N‐Acetylaspartic acid promotes oxidative stress in cerebral cortex of rats

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