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Induced Oxidative Stress (induced + oxidative_stress)
Selected AbstractsOrally administered melatonin reduces oxidative stress and proinflammatory cytokines induced by amyloid- , peptide in rat brain: a comparative, in vivo study versus vitamin C and EJOURNAL OF PINEAL RESEARCH, Issue 2 2003Sergio Rosales-Corral Abstract: To determine the efficacy of antioxidants in reducing amyloid- , -induced oxidative stress, and the neuroinflammatory response in the central nervous system (CNS) in vivo, three injections of fibrillar amyloid- , (fA,) or artificial cerebrospinal fluid (aCSF) into the CA1 region of the hippocampus of the rat were made. Concomitantly, one of the three free radical scavengers, i.e. melatonin, vitamin C, or vitamin E was also administered. Besides being a free radical scavenger, melatonin also has immunomodulatory functions. Antioxidant treatment reduced significantly oxidative stress and pro-inflammatory cytokines. There were no marked differences between melatonin, vitamin C, and vitamin E regarding their capacity to reduce nitrites and lipoperoxides. However, melatonin exhibited a superior capacity to reduce the pro-inflammatory response induced by fA,. [source] Prophylaxis with Centella asiatica confers protection to prepubertal mice against 3-nitropropionic-acid-induced oxidative stress in brainPHYTOTHERAPY RESEARCH, Issue 6 2010George K. Shinomol Abstract While the usage of Centella asiatica (CA) is on the increase worldwide, evidence demonstrating its protective efficacy against neurotoxicants is scarce. Hence the present study aimed to understand the neuroprotective efficacy of a standardized aqueous extract of CA against 3-nitropropionic-acid(3-NPA)-induced oxidative stress in the brain of prepubertal mice. We assessed the degree of oxidative stress in cytoplasm of brain regions of male mice (4,wk- old) given CA prophylaxis (5,mg/kg bw) for 10 days followed by 3-NPA administration (i.p.75,mg/kg bw) on the last 2 days. The neurotoxicant elicited marked oxidative stress in the brain of untreated mice as evident by enhanced malondialdehyde levels, reactive oxygen species (ROS) generation, hydroperoxides and protein carbonyls (a measure of protein oxidation) in striatum and other regions (cortex, cerebellum and hippocampus), while CA prophylaxis completely ameliorated the 3-NPA- induced oxidative stress. Depletion of glutathione (GSH) levels, total thiols, perturbations in antioxidant enzymes and cholinergic enzymes in brain discernible among 3-NPA-treated mice were predominantly restored to normalcy with CA prophylaxis. It is hypothesized that the prophylactic protection offered by CA extract against neurotoxicant exposure may be largely due to its ability to enhance GSH, thiols and antioxidant defenses in the brain of prepubertal mice. Copyright © 2009 John Wiley & Sons, Ltd. [source] Protective effects of steroids from Allium chinense against H2O2 -induced oxidative stress in rat cardiac H9C2 cellsPHYTOTHERAPY RESEARCH, Issue 3 2010Gang Ren Abstract Allium chinense, a traditional herbal medicine, has been used for the treatment of cardiovascular diseases for hundreds of years. In this study, A. chinense steroids (ACSs) including three steroidal glycosides and their parent aglycones were isolated from the bulbs of A. chinense. For the first time, their cardioprotective effects were evaluated in cultured rat cardiac H9C2 cells by pretreatment with ACSs for 24,h before exposure to 0.2,mm H2O2. The results showed the cell viability decreased markedly when H9C2 cells were incubated with 0.2,mm H2O2 alone for 2,h, while the cell lipid peroxidation (estimated by the excessive production of nitric oxide and malondialdehyde) and intracellular free calcium concentration ([Ca2+]i) increased significantly. The addition of 20,,m (below the toxic concentration) of ACSs notably attenuated the cellular injury induced by H2O2. The effects of ACSs in our experiments were similar to those of nimodipine, a clinically applied calcium channel blocker. Preliminary analysis of the structure,activity relationship indicated that ACSs with a spirostane-type skeleton exhibited stronger protection than that with a furostane-type skeleton, and glycosylation of the steroids could substantially lower the protective activities. The above results suggested the protective effects of steroids originated from A. chinense on the oxidative injury of H9C2 cells and ACSs may have potential for preventing cardiac injuries induced by oxidative stress. Copyright © 2009 John Wiley & Sons, Ltd. [source] Neuroprotective effects of Triticum aestivum L. against ,-Amyloid-induced cell death and memory impairmentsPHYTOTHERAPY RESEARCH, Issue 1 2010Jung-Hee Jang Abstract ,-Amyloid (A,) is a key component of senile plaques, neuropathological hallmarks of Alzheimer's disease (AD) and has been reported to induce cell death via oxidative stress. This study investigated the protective effects of Triticum aestivum L. (TAL) on A,-induced apoptosis in SH-SY5Y cells and cognitive dysfunctions in Sprague-Dawley (SD) rats. Cells treated with A, exhibited decreased viability and apoptotic features, such as DNA fragmentation, alterations in mitochondria and an increased Bax/Bcl-2 ratio, which were attenuated by TAL extract (TALE) pretreatment. To elucidate the neuroprotective mechanisms of TALE, the study examined A,-induced oxidative stress and cellular defense. TALE pretreatment suppressed A,-increased intracellular accumulation of reactive oxygen species (ROS) via up-regulation of glutathione, an essential endogenous antioxidant. To further verify the effect of TALE on memory impairments, A, or scopolamine was injected in SD rats and a water maze task conducted as a spatial memory test. A, or scopolamine treatment increased the time taken to find the platform during training trials, which was decreased by TALE pretreatment. Furthermore, one of the active components of TALE, total dietary fiber also effectively inhibited A,-induced cytotoxicity and scopolamine-caused memory deficits. These results suggest that TALE may have preventive and/or therapeutic potential in the management of AD. Copyright © 2009 John Wiley & Sons, Ltd. [source] Antioxidative effects of 7-hydroxy-3-methoxy-cadalene extracted from Zelkova serrata on 4-(methylinitros amino)-1-(3-pyridyl)-1-butanone-induced oxidative stress in A/J micePHYTOTHERAPY RESEARCH, Issue 5 2004J. H. Kim Abstract Effects of 7-hydroxy-3-methoxy-cadalene (cadalene) extracted from Zelkova serrata on 4-(methylinitrosamino)-1-(3-pyridyl)-1-butanone (NNK)-induced oxidative stress were examined using A/J mice. NNK (65 µg/ml water) was orally administered to 20 mice for 7 weeks, followed by free feeding of a commercial diet, not containing cadalene, for 2 weeks. The control group was maintained without NNK and cadalene administration, and treatment groups with NNK and cadalene (6.25, 25, 100 mg/kg feed) feeding for 25 weeks. The glutathione concentration of cadalene-treated (65 µg/ml water) group was signi,cantly higher than that of the group treated only with NNK (p < 0.05). The results of our study strongly indicate that cadalene exerts antioxidative effect on NNK-induced lung tumorigenesis in A/J mice. Copyright © 2004 John Wiley & Sons, Ltd. [source] Oxidative stress in SEPN1 -related myopathy: From pathophysiology to treatment,ANNALS OF NEUROLOGY, Issue 6 2009Sandrine Arbogast PhD Objective Mutations of the selenoprotein N gene (SEPN1) cause SEPN1 -related myopathy (SEPN1-RM), a novel early-onset muscle disorder formerly divided into four different nosological categories. Selenoprotein N (SelN) is the only selenoprotein involved in a genetic disease; its function being unknown, no treatment is available for this potentially lethal disorder. Our objective was to clarify the role of SelN and the pathophysiology of SEPN1-RM to identify therapeutic targets. Methods We established and analyzed an ex vivo model of SelN deficiency using fibroblast and myoblast primary cultures from patients with null SEPN1 mutations. DCFH assay, OxyBlot, Western blot, Fura-2, and cell survival studies were performed to measure intracellular oxidant activity, oxidative stress markers, calcium handling, and response to exogenous treatments. Results SelN-depleted cells showed oxidative/nitrosative stress manifested by increased intracellular oxidant activity (reactive oxygen species and nitric oxide) and/or excessive oxidation of proteins, including the contractile proteins actin and myosin heavy chain II in myotubes. SelN-devoid myotubes showed also Ca2+ homeostasis abnormalities suggesting dysfunction of the redox-sensor Ca2+ channel ryanodine receptor type 1. Furthermore, absence of SelN was associated with abnormal susceptibility to H2O2 -induced oxidative stress, demonstrated by increased cell death. This cell phenotype was restored by pretreatment with the antioxidant N-acetylcysteine. Interpretation SelN plays a key role in redox homeostasis and human cell protection against oxidative stress. Oxidative/nitrosative stress is a primary pathogenic mechanism in SEPN1-RM, which can be effectively targeted ex vivo by antioxidants. These findings pave the way to SEPN1-RM treatment, which would represent a first specific pharmacological treatment for a congenital myopathy. Ann Neurol 2009;65:677,686 [source] Oxidative Stress Alters Creatine Kinase System in Serum and Brain Regions of Polychlorinated Biphenyl (Aroclor 1254)-Exposed Rats: Protective Role of MelatoninBASIC AND CLINICAL PHARMACOLOGY & TOXICOLOGY, Issue 2 2009Prabhu Venkataraman Creatine kinase plays a key role in energy metabolism of nervous tissue and might be one of the targets for reactive oxygen species. Melatonin, an indoleamine, plays an important role in neurodegenerative diseases as an antioxidant and neuroprotector. The objective of the present study was to investigate the protective role of melatonin on polychlorinated biphenyl (Aroclor 1254)-induced oxidative stress and the changes in creatine kinase activity in brain regions of adult rats. Group I: rats were intraperitoneally (i.p.) administered with corn oil (vehicle) for 30 days. Group II: rats injected i.p. with Aroclor 1254 at 2 mg/kg body weight (bw)/day for 30 days. Groups III and IV: rats i.p. received melatonin (5 or 10 mg/kg bw/day) simultaneously with Aroclor 1254 for 30 days. After 30 days, rats were killed and the brain regions were dissected to cerebral cortex, cerebellum and hippocampus. Lipid peroxidation, hydroxyl radical and hydrogen peroxide (H2O2) levels were determined. The activity of creatine kinase was assayed in serum and brain regions, and its isoenzymes in serum were separated electrophoretically. Activity of creatine kinase was decreased while an increase in H2O2, hydroxyl radical and lipid peroxidation was observed in brain regions of polychlorinated biphenyl-treated rats. Also polychlorinated biphenyl exposure showed a significant increase in serum creatine kinase level and its isoforms such as BB-creatine kinase, MB-creatine kinase, and MM-creatine kinase. Administration of melatonin prevented these alterations induced by polychlorinated biphenyl by its free radical scavenging mechanism. Thus, polychlorinated biphenyl alters creatine kinase activity by inducing oxidative stress in brain regions, which can be protected by melatonin. [source] Effects on Lipid Peroxidation and Antioxidative Enzymes of Euonymus alatus in Cultured Rat HepatocytesBASIC AND CLINICAL PHARMACOLOGY & TOXICOLOGY, Issue 1 2009Kyung-Woon Kim In this paper, we investigate the effects of E. alatus on cultured hepatocyte cell system and lipid peroxidation in hydrogen peroxide (H2O2) treatment conditions. The study covers the physiological activity (the antioxidative activity and the nitrite-scavenging effect) of E. alatus. H2O2 that can produce intracellular free radical was used for inducer of the peroxidation of cellular lipids. Treatment of E. alatus attenuated in cell killing enhanced by increasing concentrations of H2O2. The increased malondialdehyde level induced by H2O2 treatment was reduced by pre-treatment of E. alatus. Furthermore, addition of E. alatus in cell culture medium significantly reduced cell killing and content of intracellular antioxidants. Changes in nitrite-scavenging effect of E. alatus at various concentrations (5,25 mg/ml) and various pH levels (pH 1.2, 4.2 and 6.0) were also observed. The present study was also done to investigate the effects of E. alatus on cultured hepatocyte cell system, H2O2 -induced cytotoxicity and antioxidative enzyme activities, including catalase, superoxide dismutase, glutathione peroxidase and glutathione S-transferase in H2O2 treatment conditions. E. alatus treatment had significant protective or elevating activities on these antioxidative enzyme activities compared to a normal group. The results indicate that E. alatus provides a strong antioxidant protection of cells against H2O2 -induced oxidative stress. [source] | ||||||||||