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Santy Daya - One of the best experts on this subject based on the ideXlab platform.
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antioxidant and iron binding properties of curcumin capsaicin and s allylcysteine reduce oxidative stress in rat Brain Homogenate
Journal of Agricultural and Food Chemistry, 2008Co-Authors: Amichand Dairam, Santy Daya, Ronen Fogel, Janice LimsonAbstract:Research demonstrates that antioxidants and metal chelators may be of beneficial use in the treatment of neurodegenerative diseases, such as Alzheimer’s disease (AD). This study investigated the antioxidant and metal-binding properties of curcumin, capsaicin, and S-allylcysteine, which are major components found in commonly used dietary spice ingredients turmeric, chilli, and garlic, respectively. The DPPH assay demonstrates that these compounds readily scavenge free radicals. These compounds significantly curtail iron- (Fe2+) and quinolinic acid (QA)-induced lipid peroxidation and potently scavenge the superoxide anion generated by 1 mM cyanide in rat Brain Homogenate. The ferrozine assay was used to measure the extent of Fe2+ chelation, and electrochemistry was employed to measure the Fe3+ binding activity of curcumin, capsaicin, and S-allylcysteine. Both assays demonstrate that these compounds bind Fe2+ and Fe3+ and prevent the redox cycling of iron, suggesting that this may be an additional method thr...
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non steroidal anti inflammatory agents tolmetin and sulindac attenuate oxidative stress in rat Brain Homogenate and reduce quinolinic acid induced neurodegeneration in rat hippocampal neurons
Metabolic Brain Disease, 2006Co-Authors: Amichand Dairam, Prakash Chetty, Santy DayaAbstract:Alzheimer's disease (AD) is the most common form of neurodegenerative disease in the elderly. Anti-inflammatory agents have been shown to be beneficial in preventing neurodegenerative disorders such as AD. In this study we investigated the possible antioxidant and neuroprotective properties of two non-steroidal anti-inflammatory drugs (NSAIDS), tolmetin and sulindac, using quinolinic acid (QA)-induced neurotoxicity as a model. We used the thiobarbituric acid assay to measure the extent of lipid peroxidation and the nitroblue tetrazolium assay to measure the superoxide anion generated in rat Brain Homogenate. QA (1 mM) induced lipid peroxidation in rat Brain Homogenate was significantly curtailed by co-treatment of the Homogenate with tolmetin and/or sulindac. Tolmetin and sulindac both reduced the generation of superoxide anions by the known neurotoxin, potassium cyanide (KCN). Intrahippocampal injections of QA induced neurotoxicity in rat hippocampus. N-Methyl-D-Aspartate (NMDA) receptor counts were conducted do give an indication of the amount protection offered by the NSAIDS. QA drastically reduced the number of NMDA binding sites by approximately 37%. This sharp decrease was considerably attenuated by the pre-treatment of the rats with tolmetin and sulindac (5 mg/kg/bd for five days). This study shows the antioxidant and neuroprotective properties of tolmetin and sulindac and hereby postulates that these drugs have important implications in the prevention or treatment of neurodegenerative diseases such as AD.
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indomethacin reduces lipid peroxidation in rat Brain Homogenate by binding fe2
Metabolic Brain Disease, 2003Co-Authors: Shailendra Anoopkumardukie, Barbara Lack, Kerry L Mcphail, Tebello Nyokong, Zaynab Lambat, Deepa S Maharaj, Santy DayaAbstract:One of the hallmarks of Alzheimer's disease (AD) is the progressive degeneration of cholinergic neurons in the cerebral cortex and hippocampus. It is generally accepted that this neuronal degeneration is due to free-radical-induced damage. These free radicals attack vital structural components of the neurons. This implies that agents that reduce free radical generation could potentially delay the progression of AD. Free radical generation in the Brain is assisted by the presence of iron, required by the Fenton reaction. Thus, agents that reduce iron availability for this reaction could potentially reduce free radical formation. Since non steroidal anti-inflammatory drugs (NSAIDS) have been shown to reduce the severity of AD, we investigated the possible mechanism by which indomethacin could afford neuroprotection. Our results show that indomethacin (1 mM) is able to reduce the iron-induced rise in lipid peroxidation in rat Brain Homogenates. In addition, our NMR data indicate that indomethacin binds the Fe2+/Fe3+ ion. This was confirmed by a study using UV/Vis spectrophotometry. The results imply that indomethacin provides a neuroprotective effect by binding to iron and thus making it unavailable for free radical production.
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cyanide induced free radical production and lipid peroxidation in rat Brain Homogenate is reduced by aspirin
Metabolic Brain Disease, 2000Co-Authors: Santy Daya, Roderick B Walker, Shailendra AnoopkumardukieAbstract:The neuroprotective properties of aspirin were investigated using cyanide-induced neurotoxicity as model. Cyanide, a known neurotoxic agent significantly increased lipid peroxidation and superoxide anion levels in rat Brain Homogenate in a concentration-dependent manner (0.25-1.0 mM). When Homogenate, containing 1.0 mM KCN was co-treated with aspirin (1.0 mM) there was a significant decrease in lipid peroxidation. Aspirin (0.5 mM and 1.0 mM) also significantly reduced KCN-induced superoxide anion generation. The results of the present report therefore indicate a neuroprotective role for aspirin.
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Melatonin Reduces Quinolinic Acid-Induced Lipid Peroxidation in Rat Brain Homogenate
Metabolic brain disease, 1999Co-Authors: Garrick Southgate, Santy DayaAbstract:The protective effects of melatonin against the neurotoxin, quinolinic acid, were investigated in rat Brain Homogenate using the thiobarbituric acid assay. Quinolinic acid increased lipid peroxidation in a dose dependent manner. When Homogenate was co-treated with melatonin there was a significant decrease in lipid peroxidation. The results of the present report show that melatonin may play a protective role in the Brain against the neurohormone quinolinic acid, which has been identified as a causative agent in Huntington's Disease.
Shizuo Toda - One of the best experts on this subject based on the ideXlab platform.
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inhibitory effects of phenylpropanoid metabolites on copper induced protein oxidative modification of mice Brain Homogenate in vitro
Biological Trace Element Research, 2002Co-Authors: Shizuo TodaAbstract:We present the results of an in vitro investigation of the inhibitory effects of phenylpropanoid metabolites on copper-induced protein oxidative modification of mice Brain Homogenate. The effects of caffeic acid, 3-(3, 4-dihydroxyphenyl)-l-alanine, esculetin, ferulic acid, and scopoletin were stronger than that of mannitol as a free-radical scavenger, whereas the effects of other phenylpropanoid metabolites, cinnamic acid, coniferyl alcohol, p-coumaric acid, coumarin, phenylalanine, tyrosine, and umbelliferone, were weak. These results demonstrated that phenolic carboxylic acids with 3,4-dihydroxy or 4-hydroxy-3-methoxy substituents and benzo-α-pyrons with 6,7-dihydroxy or 7-hydroxy-6-methoxy substituents in phenylpropanoid metabolites inhibit metal-induced protein oxidative modification of the Brain.
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inhibitory effects of aromatic herbs on lipid peroxidation and protein oxidative modification of mice Brain Homogenate by copper in vitro
Phytotherapy Research, 2001Co-Authors: Shizuo TodaAbstract:Several aromatic herbs were inferred to have inhibitory effects on the generation of oxygen free radicals. It has been demonstrated that free radicals produced by copper produce lipid peroxidation and protein oxidative modification in the Brain. The results presented here showed that several aromatic herbs, Caryophylli flos, Cinnamomi cortex, Foeniculi fructus and Zedoariae rhizoma, have inhibitory effects on lipid peroxidation or protein oxidative modification of mice Brain Homogenate produced by copper in vitro.
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inhibitory effects of licoisoflavones a and b and sophoraisoflavone a of sophra mooracroftiana beth ex baker on copper ion induced protein oxidative modification of mice Brain Homogenate in vitro
Biological Trace Element Research, 2001Co-Authors: Shizuo Toda, Yoshiaki ShiratakiAbstract:We present the results of an in vitro investigation of the inhibitory effects of licoisoflavones A and B and sophoraisoflavone A isolated from Sophra mooracroftiana BETH ex BAKER on copper-induced protein oxidative modification of mice Brain Homogenate in vitro. Although inhibitory effect of sophoraisoflavone A was stronger than those of licoisoflavones A and B, genistein as a related isoflavone, and mannitol as a hydroxy radical scavenger, inhibitory effects of licoisoflavones A and B were weaker than those of genistein and mannitol. These results demonstrated that the difference of inhibitory effects are dependent on the relation between chemical structures of these isoflavones, such as hydroxy group or benzopyran, and oxidative stress.
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Inhibitory effects of echinoisoflavanone and sophoraisoflavanone D in Sophora chrysophylla SEEM on lipid peroxidation of mice Brain Homogenate by interaction of ferrous ion and hydrogen peroxide, in vitro
Biological Trace Element Research, 2001Co-Authors: Shizuo Toda, Yoshiaki ShiratakiAbstract:We present the results of an in vitro investigation of the inhibitory effects of echinoisoflavanone and sophoraisoflavanone D isolated from Sophora chrysophylla SEEM on lipid peroxidation of mice Brain Homogenate by interaction of ferrous ion and hydrogen peroxide, in vitro. They inhibited lipid peroxidation. The order of inhibitory effects of these isoflavanones and mannitol as a hydroxy radical scavenger was echinoisoflavanone > mannitol > sophoraisoflavanone D. The results suggest that some isoflavanones may be of use in cases where oxidative stress is present.
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inhibitory effects of ougi keishi gomotsu to a traditional herbal medicine on lipid peroxidation and protein oxidative modification of mouse Brain Homogenate induced by copper
Phytotherapy Research, 1999Co-Authors: Shizuo Toda, Yoshiro YaseAbstract:Ougi-Keishi-gomotsu-to a traditional herbal medicine, is used clinically for patients with abnormal sensations and pain in the legs in neuropathy. It was shown to have inhibitory effects on lipid peroxidation and protein oxidative modification of Brain Homogenate induced by copper. Its effect was stronger than those of mannitol and α-tocopherol as free radical scavenger and antioxidant. These results demonstrated that Ougi-keishi-gomotsu-to has antioxidative effects on neuron injury derived from oxidative stress induced by metal. Copyright © 1999 John Wiley & Sons, Ltd.
Yoshiro Yase - One of the best experts on this subject based on the ideXlab platform.
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inhibitory effects of ougi keishi gomotsu to a traditional herbal medicine on lipid peroxidation and protein oxidative modification of mouse Brain Homogenate induced by copper
Phytotherapy Research, 1999Co-Authors: Shizuo Toda, Yoshiro YaseAbstract:Ougi-Keishi-gomotsu-to a traditional herbal medicine, is used clinically for patients with abnormal sensations and pain in the legs in neuropathy. It was shown to have inhibitory effects on lipid peroxidation and protein oxidative modification of Brain Homogenate induced by copper. Its effect was stronger than those of mannitol and α-tocopherol as free radical scavenger and antioxidant. These results demonstrated that Ougi-keishi-gomotsu-to has antioxidative effects on neuron injury derived from oxidative stress induced by metal. Copyright © 1999 John Wiley & Sons, Ltd.
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effect of aluminum on iron induced lipid peroxidation and protein oxidative modification of mouse Brain Homogenate
Biological Trace Element Research, 1998Co-Authors: Shizuo Toda, Yoshiro YaseAbstract:In the present study the authors report on the enhancing effect of aluminum(III) (Al[III]) on iron(II)(Fe[II])-induced lipid peroxidation (LPO) of mice Brain Homogenate, which occurs in a concentration and time-dependent manner. No evidence of LPO caused by Al alone was found.
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Inhibitory effects of Keishi-bukuryo-gan, a traditional herbal medicine, on lipid peroxidation of Brain Homogenate
Phytotherapy Research, 1996Co-Authors: Shizuo Toda, M. Ohnishi, M. Tsuduki, Yoshiro YaseAbstract:Keishi-bukuryo-gan, a traditional herbal medicine, is a representative drug for blood stagnation and an effective drug for Brain disorders. Keishi-bukuryo-gan was shown to have inhibitory effects on lipid peroxidation of Brain Homogenate induced by the ferrous ion-hydrogen peroxide system. This drug inhibited lipid peroxidation of Brain Homogenate in a concentration-dependent manner. This effect was similar to that of DL-α-tocopherol as an antioxidant.
A Mori - One of the best experts on this subject based on the ideXlab platform.
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free radical scavenging by Brain Homogenate implication to free radical damage and antioxidant defense in Brain
Neurochemistry International, 1994Co-Authors: A Mori, Jiankang Liu, Xiaoyan Wang, Motoko KawaiAbstract:Abstract To study the mechanisms of free radical-induced Brain damage and the antioxidant defense in the Brain, we quantified the superoxide and hydroxyl radical scavenging effects of Brain Homogenate using electron spin resonance spectrometry. Brain Homogenate was found to scavenge both superoxide and hydroxyl radicals in concentration-dependent fashion. Heat denaturation significantly decreased these scavenging effects. The ability of Brain Homogenate to scavenge free radicals implies that Brain damage can be induced by free radicals since they are known to react virtually with any type of molecule such as nucleic acids, membrane lipids, and proteins in the Brain. On the other hand, some molecules which can be regenerated or repaired after free radical scavenging are considered to be antioxidants which include both enzymatic and non-enzymatic antioxidants. Measurement of the decrease in antioxidant activity following heat denaturation suggests that the contribution of enzymatic antioxidants is about 20–40% in scavenging superoxide radicals and about 10–20% in scavenging hydroxyl radicals.
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monoamine metabolism provides an antioxidant defense in the Brain against oxidant and free radical induced damage
Archives of Biochemistry and Biophysics, 1993Co-Authors: A MoriAbstract:We propose that the Brain monoamine metabolism is one of the protective systems against oxidant- and free radical-induced damage in Brain. In the present study, we show that norepinephrine (NE), dopamine (DA), dihydroxyphenylacetic acid (DOPAC), homovanillic acid (HVA), serotonin (5-HT), and 5-hydroxyindole acetic acid (5-HIAA) protect Brain Homogenate and mitochondria against iron-dependent lipid peroxidation and protect Brain microsomes against both iron-dependent and iron-independent lipid peroxidation. These compounds protect deoxyribose and benzoate against free radical-induced degradation and aromatic hydroxylation. Electron spin resonance studies show that the monoamines are excellent scavengers or inhibitors of 1,1-diphenyl-2-picryl hydrazyl radicals in organic solution, of super-oxide and hydroxyl radicals in aqueous solution, and of carbon-centered radicals induced by iron ions in Brain Homogenate. Pro-oxidant properties were found in Fe(II)-H2O2-induced glutamic acid and 2-aminobutyric acid degradation, and confirmed in Fe(III)-bleomycin-dependent DNA degradation in a biphasic manner. The above effects are approximately in the order of NE = DA = 5-HT; DA > DOPAC > HVA; and 5-HT > 5-HIAA.Related supportive and contrary observations and hypotheses are discussed. Attempts are also made to briefly interpret some experimental and clinical observations.
Hideo Iwahashi - One of the best experts on this subject based on the ideXlab platform.
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identification of a radical formed in the reaction mixture of rat Brain Homogenate with a ferrous ion ascorbic acid system using hplc epr and hplc epr ms
Free Radical Research, 2007Co-Authors: Kazumasa Kumamoto, Tomihiro Hirai, Shiroh Kishioka, Hideo IwahashiAbstract:Identification of a free radical is performed for the reaction mixture of rat Brain Homogenate with a ferrous ion/ascorbic acid system using EPR, high performance liquid chromatography-electron paramagnetic resonance spectrometry (HPLC-EPR) and high performance liquid chromatography-electron paramagnetic resonance-mass spectrometry (HPLC-EPR-MS). EPR measurements of the reaction mixtures showed prominent signals with hyperfine coupling constants (alpha(N) = 1.58 mT and alpha(H)beta = 0.26 mT). No EPR spectrum was detectable without rat Brain Homogenate, suggesting that the radical is derived from rat Brain Homogenate. An HPLC-EPR analysis of the reaction mixture showed a peak with retention time of 33.7 min. An HPLC-EPR-MS analysis of the peak gave two ions at m/z 224 and 137, suggesting that alpha-(4-pyridyl-1-oxide)-N-tert-butylnitrone (4-POBN)/ethyl radical adduct forms in the reaction mixture.