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Antioxidant Agent (antioxidant + agent)

Distribution by Scientific Domains

Medical Sciences	50%
Life Sciences	21%
Chemistry	21%

Selected Abstracts

Thieno[2,3- d]pyrimidines in the Synthesis of Antitumor and Antioxidant Agents

ARCHIV DER PHARMAZIE, Issue 5 2010
Ashraf A. Aly
Abstract Dimethyl acetylenedicarboxylate, ethyl propiolate, and E -dibenzoylethylene react with thienopyrimidines (cyclo-pentyl, -hexyl, and -heptyl) derivatives to form thiazolo[3,2- a]thieno-[2,3- d]pyrimidin-2-ylidene) acetates, thieno[2,3- d]pyrimidin-2-ylthioacrylates, and thieno[2,,3,:4,5]pyrimido[2,1- b][1,3]thiazin-6-ones, respectively. Reactions proceed via cyclization and thio-addition processes. Some derivatives of thienopyrimidines showed high inhibition of Hep-G2 cell growth compared with the growth of untreated control cells. However, the fused heptyl of thienopyrimidothiazines indicates a promising specific antitumor agent against Hep-G2 cells with IC50 < 20 ,M. [source]

Synthesis and biological evaluation of new benzo[f]furo[2,3- h]-and benzo[f]pyrano[2,3- h]coumarin derivatives. ,

JOURNAL OF HETEROCYCLIC CHEMISTRY, Issue 3 2007
Maria Tsoukka
Furocoumarins 3,5 and pyranocoumarin 7 were synthesized from the reaction of furonaphthalenediones 2,4 and pyranonaphthalenedione 6 respectively with carbethoxymethylene(triphenyl)phosphorane in refluxing DCM for 3-6 hours or under microwave irradiation in toluene for a few minutes. Compounds 3,5,7 and their precursors were tested as anti-inflammatory/antioxidant agents. They were found to compete significantly high DMSO for OH radicals, to scavenge O2, and to inhibit lipoxygenase to a high extent. [source]

Effect of vitamin E supplementation in patients with ataxia with vitamin E deficiency

EUROPEAN JOURNAL OF NEUROLOGY, Issue 5 2001
S. Gabsi
Ataxia with vitamin E (Vit E) defciency (AVED) is an autosomal recessive disorder caused by mutations of the , tocopherol transfer protein gene. The Friedreich ataxia phenotype is the most frequent clinical presentation. In AVED patients, serum Vit E levels are very low in the absence of intestinal malabsorption. As Vit E is a major antioxidant agent, Vit E deficiency is supposed to be responsible for the pathological process. Twenty-four AVED patients were fully investigated (electromyography, nerve conduction velocity (NVC) studies, somatosensory evoked potentials, cerebral computed tomography scan, sural nerve biopsy, genetic studies) and supplemented with Vit E (800 mg daily) during a 1-year period. Clinical evaluation was mainly based on the Ataxia Rating Scale (ARS) for cerebellar ataxia assessment and serum Vit E levels were monitored. Serum Vit E levels normalized and ARS scores decreased moderately but significantly suggesting clinical improvement. Better results were noted with mean disease duration , 15 years. Reflexes remained abolished and posterior column disturbances unchanged. Vitamin E supplementation in AVED patients stabilizes the neurological signs and can lead to mild improvement of cerebellar ataxia, especially in early stages of the disease. [source]

Excitotoxic damage, disrupted energy metabolism, and oxidative stress in the rat brain: antioxidant and neuroprotective effects of l -carnitine

JOURNAL OF NEUROCHEMISTRY, Issue 3 2008
Daniela Silva-Adaya
Abstract Excitotoxicity and disrupted energy metabolism are major events leading to nerve cell death in neurodegenerative disorders. These cooperative pathways share one common aspect: triggering of oxidative stress by free radical formation. In this work, we evaluated the effects of the antioxidant and energy precursor, levocarnitine (l -CAR), on the oxidative damage and the behavioral, morphological, and neurochemical alterations produced in nerve tissue by the excitotoxin and free radical precursor, quinolinic acid (2,3-pyrindin dicarboxylic acid; QUIN), and the mitochondrial toxin, 3-nitropropionic acid (3-NP). Oxidative damage was assessed by the estimation of reactive oxygen species formation, lipid peroxidation, and mitochondrial dysfunction in synaptosomal fractions. Behavioral, morphological, and neurochemical alterations were evaluated as markers of neurotoxicity in animals systemically administered with l -CAR, chronically injected with 3-NP and/or intrastriatally infused with QUIN. At micromolar concentrations, l -CAR reduced the three markers of oxidative stress stimulated by both toxins alone or in combination. l -CAR also prevented the rotation behavior evoked by QUIN and the hypokinetic pattern induced by 3-NP in rats. Morphological alterations produced by both toxins (increased striatal glial fibrillary acidic protein-immunoreactivity for QUIN and enhanced neuronal damage in different brain regions for 3-NP) were reduced by l -CAR. In addition, l -CAR prevented the synergistic action of 3-NP and QUIN to increase motor asymmetry and depleted striatal GABA levels. Our results suggest that the protective properties of l -CAR in the neurotoxic models tested are mostly mediated by its characteristics as an antioxidant agent. [source]

Melatonin improves oxidative stress parameters measured in the blood of elderly type 2 diabetic patients

JOURNAL OF PINEAL RESEARCH, Issue 3 2009
Kornelia K, dziora-Kornatowska
Abstract:, An elevated oxidative status in the aging organism may be involved in the development of non-insulin dependent diabetes mellitus (NIDDM). Melatonin, a potent antioxidant agent, is essential for glucose homeostasis and regulation. The aim of this study was to determine the influence of melatonin supplementation on the oxidative stress parameters in elderly NIDDM patients. The malondialdehyde (MDA) concentration, Cu-Zn superoxide dismutase (SOD-1) activity in erythrocytes, the level of nitrate/nitrite in plasma and morning melatonin concentration and oxidase activity of ceruloplasmin (Cp) in serum in 15 elderly NIDDM patients at baseline and after the 30 days of melatonin supplementation (5 mg daily) in comparison with levels in 15 healthy elderly volunteers were determined. A significant increase of MDA level and decrease of SOD-1 activity and melatonin concentration were observed in NIDDM patients. Cp oxidase activity and nitrate/nitrite level were similar in both examined groups. Melatonin administration in NIDDM patients resulted in a significant increase in the morning melatonin concentration and SOD-1 activity, and a reduction in the MDA level and Cp oxidase activity. Statistically significant alterations in nitrate/nitrite levels were not observed. These results indicate an improvement of antioxidative defense after melatonin supplementation in the NIDDM individuals and suggest melatonin supplementation as an additional treatment for the control of diabetic complications. [source]

Melatonin protects against endosulfan-induced oxidative tissue damage in rats

JOURNAL OF PINEAL RESEARCH, Issue 4 2008
Gülden Z. Omurtag
Abstract:, Endosulfan is a chlorinated cyclodiene insecticide which induces oxidative stress. In this study, we investigated the possible protective effect of melatonin, an antioxidant agent, against endosulfan (Endo)-induced toxicity in rats. Wistar albino rats (n = 8) were administered endosulfan (22 mg/kg/day orally) followed by either saline (Endo group) or melatonin (10 mg/kg/day, Endo + Mel group) for 5 days. In other rats, saline (control group) or melatonin (10 mg/kg/day, Mel group) was injected for 5 days, following corn oil administration (vehicle of endosulfan). Measurement of malondialdehyde (MDA) and glutathione (GSH) levels, myeloperoxidase (MPO) activity and collagen content were performed in liver and kidney. Furthermore, aspartate aminotransferase (AST), alanine aminotransferase (ALT), blood urea nitrogen (BUN), and creatinine levels, lactate dehydrogenase (LDH) activity were measured in the serum samples, while tumor necrosis factor-, (TNF-,), interleukin-, (IL-,) and total antioxidant capacity (AOC) were assayed in plasma samples. Endosulfan administration caused a significant decrease in tissue GSH and plasma AOC, which was accompanied with significant rises in tissue MDA and collagen levels and MPO activity. Moreover, the proinflammatory mediators (TNF-, and IL-,), LDH activity, AST, ALT, creatinine and BUN levels were significantly elevated in the endosulfan-treated rats. On the other hand, melatonin treatment reversed all these biochemical alterations induced by endosulfan. Our results suggest that oxidative mechanisms play an important role in endosulfan-induced tissue damage and melatonin, by inhibiting neutrophil infiltration, balancing oxidant,antioxidant status and regulating the generation of inflammatory mediators, ameliorates oxidative organ injury as a result of endosulfan toxicity. [source]

Bilirubin influence on oxidative lung damage and surfactant surface tension properties

PEDIATRIC PULMONOLOGY, Issue 3 2004
Carlo Dani MD
Abstract To study the hypothesis that hyperbilirubinemia might reduce in vivo oxidative lung damage while also diminishing lung surfactant surface tension properties during acute lung injury, we performed a randomized study in a rabbit model of acute lung injury. Twenty rabbits were randomized to receive bilirubin or saline intravenously. Acute lung injury was induced by lung lavages with saline. Lung tissue oxidation was evaluated by measuring total hydroperoxide (TH), advanced oxidation protein products (AOPP), and protein carbonyls (PC) in bronchial aspirate (BA) samples. Surface surfactant activity was studied in BA samples using a capillary surfactometer. Bilirubin BA concentration increased in bilirubin-treated rabbits, while it remained undetectable in controls. A similar increase in TH, AOPP, and PC bronchial aspirate concentrations was found in both the study and control groups, while surfactant surface activity was lower in the bilirubin than in the control group. We conclude that during hyperbilirubinemia, bilirubin enters the lung tissue, where it can be detected in BA fluid. Bilirubin is not effective as an antioxidant agent and exerts a detrimental effect on lung surfactant surface tension properties. These findings may have relevance to the management of premature neonates suffering from respiratory distress syndrome and hyperbilirubinemia. Pediatr Pulmonol. © 2004 Wiley-Liss, Inc. [source]

Astragalus membranaceus prevents daunorubicin-induced apoptosis of cultured neonatal cardiomyocytes: role of free radical effect of Astragalus membranaceus on daunorubicin cardiotoxicity

PHYTOTHERAPY RESEARCH, Issue 6 2009
ZhongGuang Luo
Abstract Anthracyclines are antitumor antibiotics with significant activity against solid and hematologic malignancies. One problem preventing more widespread use has been the development of cardiotoxicity. To determine whether antioxidant agents can reduce the cardiotoxicity of anthracyclines, a herb Astragalus membranaceus was introduced, which has been widely used for the treatment of cardiovascular diseases in China and was confirmed to be an effective antioxidant agent recently. Pre-treatment with Astragalus membranaceus significantly attenuated the daunorubicin-induced increases of reactive oxygen species (p < 0.001), apoptosis (p < 0.05) and the secretions of LDH (p < 0.01) in cultured neonatal cardiomyocytes. Astragalus membranaceus also raised the EC50 of daunorubicin 1.24-fold. Compared with Astragalus membranaceus, N -acetyl- l -cysteine had similar effects on daunorubicin-induced cell injury, however, superoxide dismutase reduced reactive oxygen species without attenuating apoptosis. The subcellular distribution of DNR was similar to the distribution of MitoTracker Red 580 in mitochondria, which was mainly in the cytoplasm around the nuclear membrane in cultured neonatal cardiomyocytes. In conclusion, the results suggested that Astragalus membranaceus is potentially protective against daunorubicin cardiotoxicity by decreasing free radical release and apoptosis in cultured neonatal cardiomyocytes. The main subcellular distribution of daunorubicin may be in the mitochondria. Copyright © 2009 John Wiley & Sons, Ltd. [source]

Effects of melatonin and caffeic acid phenethyl ester on testicular injury induced by myocardial ischemia/reperfusion in rats

FUNDAMENTAL & CLINICAL PHARMACOLOGY, Issue 3 2005
Mukaddes E
Abstract Experimental studies indicate that ischemia/reperfusion (I/R) causes remote organ injury although the molecular mechanism has not been clearly defined. In this report, the role of oxidative injury on testicular damage following myocardial I/R injury and the effects of antioxidant agents, melatonin and caffeic acid phenethyl ester (CAPE), on testicular injury were investigated. As far as we know, this is the first report demonstrating that myocardial I/R induces damage to the testes. Thirty-two male Wistar rats were randomly divided into four groups: sham operation (SO), I/R + vehicle, I/R + melatonin, and I/R + caffeic acid phenethyl ester. To produce cardiac damage, the left main coronary artery was occluded for 30 min, followed by 120 min reperfusion, in anesthetized rats. Serum nitric oxide (NO) and malondialdehyde (MDA) levels and morphological changes were examined. I/R was accompanied by a significant increase in serum MDA and NO levels, whereas, melatonin and CAPE administration significantly reduced these values. Melatonin was more efficient in reducing MDA levels than CAPE (P < 0.05). I/R induced myocardial damage, manifested as the histopathological evidence of intracellular vacuolization, interstitial edema, neutrophil infiltration and coagulative necrosis. I/R + vehicle group showed many histological alterations such as focal tubular atrophy, and degeneration and disorganization of the seminiferous epithelium in testes. The number of atrophic tubules and degenerating cells was significantly higher in I/R + vehicle group than that of SO group. Melatonin and CAPE significantly reduced the number of degenerating cells; additionally, melatonin reduced the number of atrophic tubules (P < 0.05). Our results indicate that myocardial I/R induces severe testicular damage and antioxidant agents, especially melatonin, have protective effects on testicular injury after myocardial I/R. Our data emphasize that oxygen-based reactants may play a central role in remote organ injury. [source]

Mobile phase additives for enhancing the chromatographic performance of astaxanthin on nonendcapped polymeric C30 -bonded stationary phases

JOURNAL OF SEPARATION SCIENCE, JSS, Issue 1 2009
Philipp Kaiser
Abstract Astaxanthin shows peak deformation and reduced peak area response when eluted with methanol and methyl tert -butyl ether on nonendcapped polymeric C30 -bonded HPLC phases. The present study tested different column manufacturers, column batches, and ten mobile phase additives including acids, bases, buffers, complexing and antioxidant agents for improvement of peak shape and peak area response. Concerning chromatographic benefits and feasibility, ammonium acetate was found to be the best additive followed by triethylamine for all columns tested. Variation of the mobile phase pH equivalent and the column temperature showed no synergistic effects on peak shape and peak area response. Results indicate that peak tailing and variation of peak area response are due to different on-column effects. Possible mechanisms of the observed phenomenon will be discussed. [source]

Ethanol Can Modify the Effects of Certain Free Radical-Generating Systems on Astrocytes

ALCOHOLISM, Issue 4 2004
B. Gonthier
Abstract: The central nervous system is vulnerable to oxidative stress, especially when a toxicant can modify the physiological balance between anti- and pro-oxidant mechanisms. Among brain cells, astrocytes seem less vulnerable than neurons, but their impairment can dramatically affect neurons because of their protective role toward neurons. Ethanol is able to stimulate the formation of reactive oxygen species and modify the activity of most of the antioxidant agents. However, ethanol can react with the OH· radical to form the ,-hydroxyethyl radical, which is considered to be less toxic. Ethanol also can stimulate H2O2 degradation through catalase activation. This study, therefore, sought to determine whether ethanol affected the sensitivity of astrocytes exposed to various free radical-generating systems. The cellular impact of such exposure was assessed by assays exploring cytotoxicity (i.e., NR (neutral red) and MMT (3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetiazolium bromide) reduction assays) and genotoxicity (comet assay) induced by these treatments. DNA alterations were evaluated by single-cell gel electrophoresis (comet assay), considered a precocious biomarker of intracellular alterations. After concomitant exposure to H2O2 and ethanol, the viability of astrocytes decreased significantly whereas the mean percentage of DNA in the tail increased, reflecting DNA damage (H2O2 was either directly added to the culture medium or endogenously produced from menadione). Ethanol also reduced the loss of viability and DNA alterations after exposure to OH· radicals produced by a Fenton system. The exposure to a xanthine/xanthine oxidase system had the same effect. [source]

Oxidative stress in developmental brain disorders

NEUROPATHOLOGY, Issue 1 2009
Masaharu Hayashi
Oxidative stress is one of the predisposing factors in adult neurological disorders. We have examined the involvement of oxidative stress in child-onset neurodegenerative disorders, and here we review the findings from our analysis. In cases of Cockayne syndrome, the oxidative products of lipids and proteins were increased in the globus pallidus; however, oxidative nucleotide damage that coincided with reduced copper/zinc superoxide dismutase (Cu/ZnSOD) expression was observed in cases of xeroderma pigmentosum, and these patients also presented increased oxidative stress markers in urine samples. In spinal muscular atrophy, lipid peroxidation in conjunction with oxidative DNA damage was observed in motor neurons. Cases of subacute sclerosing panencephalitis presented oxidative nucleoside damage in cerebral cortical neurons at early disease stages, which were subsequently replaced by lipid peroxidation in glial cells of cerebral white matter. In relation to progressive myoclonic epilepsy, oxidative damage to DNA, proteins, and lipids appeared to coincide with cerebral and cerebellar cortical lesions of neuronal ceroid-lipofuscinosis. Patients with Lafora disease also presented an increase in oxidative stress markers for DNA and/or lipids in the brain and urine. These findings imply involvement of oxidative stress in developmental brain disorders; antioxidant agents could prove to be useful for treating patients with those disorders. [source]

Astragalus membranaceus prevents daunorubicin-induced apoptosis of cultured neonatal cardiomyocytes: role of free radical effect of Astragalus membranaceus on daunorubicin cardiotoxicity

Innovations in the Development and Application of Edible Coatings for Fresh and Minimally Processed Fruits and Vegetables

COMPREHENSIVE REVIEWS IN FOOD SCIENCE AND FOOD SAFETY, Issue 3 2007
Daniel Lin
ABSTRACT:, One of the major growth segments in the food retail industry is fresh and minimally processed fruits and vegetables. This new market trend has thus increased the demands to the food industry for seeking new strategies to increase storability and shelf life and to enhance microbial safety of fresh produce. The technology of edible coatings has been considered as one of the potential approaches for meeting this demand. Edible coatings from renewable sources, including lipids, polysaccharides, and proteins, can function as barriers to water vapor, gases, and other solutes and also as carriers of many functional ingredients, such as antimicrobial and antioxidant agents, thus enhancing quality and extending shelf life of fresh and minimally processed fruits and vegetables. This review discusses the rationale of using edible coatings on fresh and minimally processed produce, the challenges in developing effective coatings that meet the specific criteria of fruits and vegetables, the recent advances in the development of coating technology, the analytical techniques for measuring some important coating functionalities, and future research needs for supporting a broad range of commercial applications. [source]