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Superoxide Dismutase Activity (superoxide + dismutase_activity)
Selected AbstractsOxidative stress, defense response, and early biomarkers for lead-contaminated soil in Vicia faba seedlings,ENVIRONMENTAL TOXICOLOGY & CHEMISTRY, Issue 4 2008Cheng-Run Wang Abstract Chemical analyses and biological measurements were investigated in leaves of Vicia faba seedlings exposed to extraneous lead (Pb) at 0 to 2,000 mg/kg of soil for a month. The results showed that superoxide radical (O,,2) production, increased along with total Pb in leaves and available Pb in soil, resulted in enhancement of malondialdehyde and carbonyl groups. Antioxidant enzymes, including corresponding isoenzymes and heat shock protein 70 (hsp 70), were also enhanced to some extent. Significant changes were detected in the patterns and intensities of guaiacol peroxidase isoenzymes, while superoxide dismutase, catalase, and ascorbate peroxidase isoenzymes only changed intensities. Superoxide dismutase activities increased with the increase of extraneous Pb at 0 to 500 mg/kg of soil and tended to decline thereafter, which might be responsible for the decrease of hydrogen peroxide and accumulation of O,,2. Guaiacol peroxidase and ascorbate peroxidase enzymes were upregulated to become major scavengers of excess hydrogen peroxide on the condition of decreased catalase activities. Levels of hsp 70 were well correlated with Pb contents in leaves (r = 0.777), O,,2 accumulation (r = 0.985, p < 0.01), and carbonyl groups (r = 0.920, p < 0.01) under extraneous Pb at 0 to 250 mg/kg of soil, suggesting that hsp 70 induced by O,,2 was possibly involved in disposal of denatured proteins. The results showed that O,,2, hsp 70, and guaiacol peroxidase isoenzymes had the most sensitive responses in the seedlings and these parameters could be potential early biomarkers of soil Pb contamination. [source] Oral malodorous compound causes apoptosis and genomic DNA damage in human gingival fibroblastsJOURNAL OF PERIODONTAL RESEARCH, Issue 4 2008K. Yaegaki Background and Objective:, Volatile sulfur compounds are the main cause of halitosis. Hydrogen sulfide is one of these volatile sulfur compounds and the principal malodorous compound in physiological halitosis. Periodontally pathogenic activities of hydrogen sulfide have been previously reported. Hydrogen sulfide induces apoptotic cell death in aorta smooth muscle cells and in other tissues. Apoptosis plays an important role in the onset and progress of periodontitis. The objective of this study was to determine whether hydrogen sulfide causes apoptosis in human gingival fibroblasts. Material and methods:, Necrotic cells were detected using a lactate dehydrogenase assay. Apoptosis was ascertained using a histone-complexed DNA fragment assay and flow cytometry. The level of caspase 3, a key enzyme in apoptotic signaling, was also measured, and the effects of hydrogen sulfide on reactive oxygen species and superoxide dismutase were assessed. DNA damage caused by hydrogen sulfide was examined by means of single-cell gel electrophoresis. Results:, After 72 h of incubation with 100 ng/mL of hydrogen sulfide, necrosis was found in less than 10% of human gingival fibroblasts, whereas apoptosis was significantly increased (p < 0.05). Superoxide dismutase activity was strongly inhibited, and reactive oxygen species production was enhanced, after 48 and 72 h of incubation. Caspase 3 activity was also increased after 72 h of incubation (p < 0.01). Tail length, percentage of DNA in tail, and tail moment, measured by single-cell gel electrophoresis, were also intensified after 72 h of incubation (p < 0.001). Conclusion:, Hydrogen sulfide caused apoptosis and DNA damage in human gingival fibroblasts. An increased level of reactive oxygen species stimulated by hydrogen sulfide may induce apoptosis and DNA strand breaks. [source] The role of erythropoietin in the protection of gastric mucosa from indometacin-induced gastric injury and its relationship with oxidant and antioxidant parameters in ratsJOURNAL OF PHARMACY AND PHARMACOLOGY: AN INTERNATI ONAL JOURNAL OF PHARMACEUTICAL SCIENCE, Issue 1 2010Fatih Albayrak Abstract Objectives Erythropoietin has anti-oxidative and anti-inflammatory activity. We wanted to evaluate its activity in preventing damage to the gastric mucosa. Methods We examined the protective effect of erythropoietin on indometacin-induced gastric mucosa damage in the rat stomach and compared its potency with that of famotidine. We also measured effects on oxidant and antioxidant parameters in the rat stomach. Key findings Famotidine and erythropoietin 2500 and 5000 IU/kg reduced the ulcer area by 98%, 31% and 58%, respectively, compared with the indometacin group. Superoxide dismutase activity and glutathione level were decreased and myeloperoxidase activity increased in the indometacin group compared with healthy rats. Famotidine and erythropoietin at all doses increased superoxide dismutase and glutathione levels significantly compared with the indometacin group. Myeloperoxidase activity was decreased by erythropoietin and famotidine. Conclusions These results support the view that erythropoietin counteracts the effects of indometacin in inducing gastric ulcer and could be used as a an antiulcer compound. Its antiulcer effect is less potent than that of famotidine. The antiulcerogenic effects of erythropoietin may be related to its intrinsic ability to sustain the activities of free-radical scavenging enzymes and the bioavailability of glutathione. [source] Effect of Nitric Oxide Synthase Inhibitors on Lipid Peroxide Formation in Liver Caused by Endotoxin ChallengeBASIC AND CLINICAL PHARMACOLOGY & TOXICOLOGY, Issue 4 2000Shuhei Sakaguchi This study investigated the effect of nitric oxide on lipid peroxide formation during endotoxaemia. Nitric oxide synthase inhibitors NG -monomethyl-L-arginine acetate (L-NMMA, 20 mg/kg, intravenously), NG -nitro-L-arginine-methyl ester (L-NAME, 10 mg/kg, intravenously), and NG -nitro-L-arginine (L-NA, 10 mg/kg, intravenously), and a relatively selective inducible nitric oxide synthase inhibitor aminoguanidine (10 mg/kg, intravenously), did not protect against endotoxin-induced death of mice. Superoxide dismutase activity in liver 18 hr after administration of endotoxin (6 mg/kg, intraperitoneally) to L-arginine analogues (L-NMMA, L-NAME, L-NA)-treated mice was lower than in mice treated with endotoxin alone, whereas the administration of L-arginine analogues increased xanthine oxidase activity in the livers of endotoxin-injected mice compared with mice treated with endotoxin alone. In mice treated with L-arginine analogues and aminoguanidine, the levels of non-protein sulfhydryl and lipid peroxide in liver 18 hr after endotoxin injection did not show significant differences from mice treated with endotoxin alone. L-Arginine analogues and aminoguanidine had little effect on lipid peroxide formation in liver caused by endotoxin. Treatment with aminoguanidine (300 ,M) significantly inhibited endotoxin-induced intracellular peroxide in J774A.1 cells, however, aminoguanidine did not affect endotoxin-induced cytotoxicity in J774A.1 cells. Our results clearly demonstrate that treatment with catalase (10 ,g/ml), D-mannitol (10 mM), or superoxide dismutase (100 U/ml), has little or no effect on nitric oxide production by endotoxin (1 ,g/ml)-activated J774A.1 cells. These findings suggest that nitric oxide is not crucial for lipid peroxide formation during endotoxaemia. Therefore, it is unlikely that nitric oxide plays a significant role in liver injury caused by free radical generation in endotoxaemia. [source] Oxidative stress and hippocampus in a low-grade hepatic encephalopathy model: protective effects of curcuminHEPATOLOGY RESEARCH, Issue 11 2008Diego Martín Roselló Aim:, The present study was performed on prehepatic portal hypertensive rats, a model of low-grade hepatic encephalopathy, designed to evaluate whether oxidative stress was a possible pathway implicated in hippocampal damage and if so, the effect of an anti-oxidant to prevent it. Methods:, Prehepatic portal hypertension was induced by a regulated portal vein stricture. Oxidative stress was investigated by assessing related biochemical parameters in rat hippocampus. The effect of the anti-oxidant curcumin, administered in a single i.p. dose of 100 mg/kg on the seventh, ninth and eleventh days after surgery, was evaluated. Results:, Oxidative stress in the rat hippocampal area was documented. Curcumin significantly decreased tissue malondialdehyde levels and significantly increased glutathione peroxidase, catalase and superoxide dismutase activities in the hippocampal tissue of portal hypertensive rats. Conclusion:, Oxidative stress was found to be implicated in the hippocampal damage and curcumin protected against this oxidative stress in low-grade hepatic encephalopathic rats. These protective effects may be attributed to its anti-oxidant properties. [source] Panax ginseng reduces adriamycin-induced heart failure in ratsPHYTOTHERAPY RESEARCH, Issue 12 2005Jyh-Sheng You Abstract The purpose of this study was to investigate the protective effects of Panax ginseng on adriamycin-induced heart failure. Wistar rats were divided into four groups: control, adriamycin, ginseng and adriamycin with ginseng. Adriamycin (cumulative dose, 15 mg/kg) was administered to rats in six equal intraperitoneal injections over a period of 2 weeks. Ginseng was administered via an oral feeding tube once a day for 30 days (cumulative dose, 150 g/kg). At the end of the 5 week post-treatment period, the hearts of the rats were used to study the synthesis rates of DNA, RNA and protein, myocardial antioxidants and lipid peroxidation. At the end of 3 weeks treatment, heart failure was characterized by ascites, congested liver and depressed cardiac function. Nucleic acid as well as protein synthesis was inhibited, lipid peroxidation was increased and myocardial glutathione peroxidase activity was decreased indicating adriamycin-induced heart failure. In contrast, the administration of ginseng, before and concurrent with adriamycin, significantly attenuated the myocardial effects, lowered the mortality as well as the amount of ascites, increased in myocardial glutathione peroxidase, macromolecular biosynthesis and superoxide dismutase activities, with a concomitant decrease in lipid peroxidation. These findings indicated that ginseng may be partially protective against adriamycin-induced heart failure. Copyright © 2005 John Wiley & Sons, Ltd. [source] Glutathione deficiency intensifies ischaemia-reperfusion induced cardiac dysfunction and oxidative stressACTA PHYSIOLOGICA, Issue 1 2001S. Leichtweis The efficacy of glutathione (GSH) in protecting ischaemia-reperfusion (I-R) induced cardiac dysfunction and myocardial oxidative stress was studied in open-chest, stunned rat heart model. Female Sprague,Dawley rats were randomly divided into three experimental groups: (1) GSH-depletion, by injection of buthionine sulphoxamine (BSO, 4 mmol kg,1, i.p.) 24 h prior to I-R, (2) BSO injection (4 mmol kg,1, i.p.) in conjunction with acivicin (AT125, 0.05 mmol kg,1, i.v.) infusion 1 h prior to I-R, and (3) control (C), receiving saline treatment. Each group was further divided into I-R, with surgical occlusion of the main left coronary artery (LCA) for 30 min followed by 20 min reperfusion, and sham. Myocardial GSH content and GSH : glutathione disulphide (GSSG) ratio were decreased by ,50% (P < 0.01) in both BSO and BSO + AT125 vs. C. Ischaemia-reperfusion suppressed GSH in both left and right ventricles of C (P < 0.01) and left ventricles of BSO and BSO + AT125 (P < 0.05). Contractility (+dP/dt and ,dP/dt) in C heart decreased 55% (P < 0.01) after I and recovered 90% after I-R, whereas ±dP/dt in BSO decreased 57% (P < 0.01) with ischaemia and recovered 76 and 84% (P < 0.05), respectively, after I-R. For BSO + AT125, ±dP/dt were 64 and 76% (P < 0.01) lower after ischaemia, and recovered only 67 and 61% (P < 0.01) after I-R. Left ventricular systolic pressure in C, BSO and BSO + AT125 reached 95 (P > 0.05) 87 and 82% (P < 0.05) of their respective sham values after I-R. Rate-pressure double product was 11% (P > 0.05) and 25% (P < 0.05) lower in BSO and BSO + AT125, compared with Saline, respectively. BSO and BSO + AT125 rats demonstrated significantly lower liver GSH and heart Mn superoxide dismutase activity than C rats after I-R. These data indicate that GSH depletion by inhibition of its synthesis and transport can exacerbate cardiac dysfunction inflicted by in vivo I-R. Part of the aetiology may involve impaired myocardial antioxidant defenses and whole-body GSH homeostasis. [source] Changes in antioxidant defense status in response to cisplatin and 5-FU in esophageal carcinomaDISEASES OF THE ESOPHAGUS, Issue 2 2008T. Kaur SUMMARY., The ability of reactive oxygen species to induce cellular damage and to cause cell death opens the possibility of exploiting this property in the treatment of esophageal cancer through a free radical mediated mechanism. The present study was carried out with the aim of evaluating the changes in the antioxidant defense status in esophageal cancer patients treated without and with neoadjuvant therapy (NAT). Forty surgically resected tissue specimens from tumors, tissue adjoining the tumors and paired macroscopically normal mucosa were obtained from esophageal cancer patients treated with or without chemo-radiotherapy. An evaluation of antioxidant defense system in the normal, adjoining and tumor esophageal tissues in response to NAT revealed decreased catalase activity in tumor and adjoining tissues as compared to their respective normal tissue levels. Similarly, decreased superoxide dismutase activity was observed in tumor tissue in response to NAT. In both the treatment groups (with and without NAT), no significant change was observed in the enzyme activity of glutathione reductase in the normal, adjoining and tumor tissues. Enhanced glutathione peroxidase activity was found in tumor tissue, as compared to the adjoining and paired normal tissue of patients after NAT. Estimation of reduced glutathione (GSH) levels showed a significant decline in GSH levels in esophageal tumors after NAT. Depletion of GSH, an endogenous antioxidant, would elevate drug sensitivity and might predispose neoplastic cells to apoptosis in response to NAT. The antioxidant enzymes in the esophageal carcinoma thus may play an important role in influencing the final outcome upon NAT course. [source] HIP/PAP accelerates liver regeneration and protects against acetaminophen injury in mice,HEPATOLOGY, Issue 3 2005Hanh-Tu Lieu Human hepatocarcinoma-intestine-pancreas/pancreatic-associated protein HIP/PAP is a secreted C-type lectin belonging to group VII, according to Drickamer's classification. HIP/PAP is overexpressed in liver carcinoma; however, its functional role remains unclear. In this study, we demonstrate that HIP/PAP is a paracrine hepatic growth factor promoting both proliferation and viability of liver cells in vivo. First, a low number of implanted hepatocytes deriving from HIP/PAP-transgenic mice (<1:1,000) was sufficient to stimulate overall recipient severe combined immunodeficiency liver regeneration after partial hepatectomy. After a single injection of HIP/PAP protein, the percentages of bromodeoxyuridine-positive nuclei and mitosis were statistically higher than after saline injection, indicating that HIP/PAP acts as a paracrine mitogenic growth factor for the liver. Comparison of the early events posthepatectomy in control and transgenic mice indicated that HIP/PAP accelerates the accumulation/degradation of nuclear phospho,signal transducer activator transcription factor 3 and tumor necrosis factor , level, thus reflecting that HIP/PAP accelerates liver regeneration. Second, we showed that 80% of the HIP/PAP-transgenic mice versus 25% of the control mice were protected against lethal acetaminophen-induced fulminate hepatitis. A single injection of recombinant HIP/PAP induced a similar cytoprotective effect, demonstrating the antiapoptotic effect of HIP/PAP. Comparison of Cu/Zn superoxide dismutase activity and glutathione reductase-like effects in control and transgenic liver mice indicated that HIP/PAP exerts an antioxidant activity and prevents reactive oxygen species-induced mitochondrial damage by acetaminophen overdose. In conclusion, the present data offer new insights into the biological functions of C-type lectins. In addition, HIP/PAP is a promising candidate for the prevention and treatment of liver failure. (HEPATOLOGY 2005;42:618,626.) [source] Stress response of yeast candida intermedia to Cr(VI)JOURNAL OF BIOCHEMICAL AND MOLECULAR TOXICOLOGY, Issue 6 2003Polona Jamnik Abstract Stress response of yeast Candida intermedia ZIM 156 exposed to chromium(VI) was investigated. Yeast cells were treated with Cr(VI) in concentrations of 50, 100, 300 and 500 ,M in the mid-exponential growth phase. Monitoring of some bioprocess parameters during growth, specifically pO2, showed that Cr(VI) addition, specifically in concentration of 100 and partially 50 ,mol/L, increased metabolism intensity, which is connected to induced stress responses. Furthermore, oxidation of 2,,7,-dichlorofluorescin indicated increased intracellular oxidant level, specifically at 100 ,M Cr(VI) concentration. Antioxidant defense systems were further investigated. Catalase and superoxide dismutase activity was not increased in the cells exposed to the both Cr(VI) concentrations, which indicate that catalase and superoxide dismutase do not participate in cell defense systems. In contrast intracellular glutathione content in reduced form increased significantly in the cells exposed to 100 ,mol Cr(VI)/L. Therefore, we demonstrated that glutathione plays an important role in the stress response of C. intermedia to Cr(VI). © 2003 Wiley Periodicals, Inc. J Biochem Mol Toxicol 17:316,323, 2003; Published online in Wiley InterScience (www.interscience.wiley.com). DOI 10.1002/jbt.10093 [source] Low complex I content explains the low hydrogen peroxide production rate of heart mitochondria from the long-lived pigeon, Columba liviaAGING CELL, Issue 1 2010Adrian J. Lambert Summary Across a range of vertebrate species, it is known that there is a negative association between maximum lifespan and mitochondrial hydrogen peroxide production. In this report, we investigate the underlying biochemical basis of the low hydrogen peroxide production rate of heart mitochondria from a long-lived species (pigeon) compared with a short-lived species with similar body mass (rat). The difference in hydrogen peroxide efflux rate was not explained by differences in either superoxide dismutase activity or hydrogen peroxide removal capacity. During succinate oxidation, the difference in hydrogen peroxide production rate between the species was localized to the ,pH-sensitive superoxide producing site within complex I. Mitochondrial ,pH was significantly lower in pigeon mitochondria compared with rat, but this difference in ,pH was not great enough to explain the lower hydrogen peroxide production rate. As judged by mitochondrial flavin mononucleotide content and blue native polyacrylamide gel electrophoresis, pigeon mitochondria contained less complex I than rat mitochondria. Recalculation revealed that the rates of hydrogen peroxide production per molecule of complex I were the same in rat and pigeon. We conclude that mitochondria from the long-lived pigeon display low rates of hydrogen peroxide production because they have low levels of complex I. [source] Effect of Yam (Dioscorea alata Compared to Dioscorea japonica) on Gastrointestinal Function and Antioxidant Activity in MiceJOURNAL OF FOOD SCIENCE, Issue 7 2006Cheng-Chin Hsu ABSTRACT:, Effects of Chinese yam (Dioscorea alata) and Japanese yam (Dioscorea japonica) on gastrointestinal functions including intestinal microflora and intestinal enzymes' activities, as well as antioxidant protection against lipopolysaccharide (LPS)-induced oxidative damage, in Balb/cA mice were examined. In part I, mice were fed yam-supplemented diet for 4 or 8 wk, and killed with carbon dioxide. In part II, mice were fed yam-supplemented diet for 4 wk, and followed by intraperitoneal LPS treatment (i.p. 4 mg/kg bodyweight). The intake of Chinese yam and Japanese yam significantly changed intestinal microflora, in which the colony numbers of Bifidobacterium and Lactobacillus were increased and the colony numbers of Clostridium perfringens were decreased (P < 0.05). The intake of both Chinese and Japanese yams also significantly elevated the activity of leucine aminopeptidase and lipase (P < 0.05), and the activities of sucrase and maltase were increased only in 20% yam-treated groups (P < 0.05). The preintake of yam significantly alleviated subsequent LPS-induced oxidative injury by decreasing lipid oxidation level and fibronectin production and elevating superoxide dismutase activity (P < 0.05). Both Chinese and Japanese yams contained dietary fibers, polyphenols, and flavonoids, which may contribute to the observed gastrointestinal function and antioxidant protection. These results suggest that both Chinese yam and Japanese yam were beneficial for intestinal health and oxidation prevention. [source] Characterization of Phaffia rhodozyma 3A 4,8 Generated by Low-dose ,-irradiationJOURNAL OF FOOD SCIENCE, Issue 9 2004S.H. Lee ABSTRACT: Astaxanthin content, superoxide dismutase activity, catalase activity, and transmission electron microscopy (TEM) of astaxanthin-hyperproducing mutant 3A 4,8, previously isolated through repeated rounds of ,-irradiation below 10 kGy and visual screening, was examined and compared with wild strain 67,385 and parent strain 2A2N to characterize its mutant. Astaxanthin content of Phaffia rhodozyma was determined using high-performance liquid chromatography. After 10 d culture, 3A 4,8 produced 2.5 mg/g yeast, 78% higher astaxanthin content than parent strain. Mutant exhibited lower superoxide dismutase and higher catalase activities than parent strain. TEM study showed mutant had smaller-sized mitochondria than parent strain. These results indicate ,-irradiation is an effective means of mutagenesis for production of carotenoidhyperproducing mutants. [source] Altered arachidonic acid biosynthesis and antioxidant protection mechanisms in Schwann cells grown in elevated glucoseJOURNAL OF NEUROCHEMISTRY, Issue 6 2002Cristinel Mîinea Abstract In cultured Schwann cells, elevated glucose induces alterations in arachidonic acid metabolism that cause a decrease in the content of glycerophospholipid arachidonoyl-containing molecular species (ACMS). This could result from decreased de novo arachidonic acid biosynthesis, or increased arachidonic acid release from phospholipids. Incorporation of radioactive 8,11,14-eicosatrienoic acid into ACMS was lower for cells grown in 30 mm versus 5 mm glucose, consistent with a decrease in ,5 desaturase activity. However, neither basal arachidonic acid release from prelabeled cells nor stimulated generation of arachidonic acid in the presence of the reacylation inhibitor, thimerosal, the phosphotyrosine phosphatase inhibitor, bipyridyl peroxovanadium, or both together, were altered by varying the glucose concentrations, indicating that arachidonic acid turnover did not contribute to ACMS depletion. Free cytosolic NAD+/NADH decreased, whereas NADP+/NADPH remained unchanged for cells grown in elevated glucose, implying that decreased desaturase activity is a result of metabolic changes other than cofactor availability. Schwann cells in elevated glucose were susceptible to oxidative stress, as shown by increased malondialdehyde, depleted glutathione levels, and reduced cytosolic superoxide dismutase activity. Glutathione-altering compounds had no effect on ACMS levels, in contrast to N -acetylcysteine and ,-lipoic acid, which partly corrected ACMS depletion in phosphatidylcholine. These findings suggest that in the Schwann cell cultures, a high glucose level elicits oxidative stress and weakens antioxidant protection mechanisms which could decrease arachidonic acid biosynthesis and that this deficit can be partly corrected by treatment with exogenous antioxidants. [source] The orally combined neuroprotective effects of sodium ferulate and borneol against transient global ischaemia in C57 BL/6J miceJOURNAL OF PHARMACY AND PHARMACOLOGY: AN INTERNATI ONAL JOURNAL OF PHARMACEUTICAL SCIENCE, Issue 7 2010Xiao-hong Chen Abstract Objectives, This study aimed to investigate the possible modification of the neuroprotective effect of sodium ferulate, when orally co-administered with borneol, in transient global cerebral ischaemia-induced functional, histological and cellular alterations in mice. Methods, The bilateral common carotid artery occlusion was conducted in C57 BL/6J mice for 25 min. The mice were then subjected to a water maze test over an extended recovery period, followed by an assessment of neuronal loss in the CA1 region of the hippocampus (haematoxylin and eosin staining). The blood,brain barrier permeability (Evans blue tracing), brain oedema and oxidative stress were assayed and histological sections were also immunostained for gliofibrillar acid protein (GFAP) expression. Key findings, The ischaemia reperfused mice were associated with long-lasting spatial learning deficits in the absence of other behavioural impairments and with neurodegeneration in the hippocampal CA1 region. However, the histological injuries were significantly attenuated by oral co-administration of sodium ferulate and borneol. Furthermore, combined treatment with sodium ferulate and borneol resulted in a significant reduction in brain oedema, GFAP-positive cells, malonaldialdehyde levels and blood,brain barrier permeability, but an increase in superoxide dismutase activity. Conclusions, Borneol may have benefits for the neuroprotective effect of sodium ferulate against injury induced in the brain by ischaemia/reperfusion. [source] Antioxidant Protection Mechanisms And Arachidonic Acid Synthesis Are Altered In Schwann Cells Grown In Elevated GlucoseJOURNAL OF THE PERIPHERAL NERVOUS SYSTEM, Issue 3 2000C Miinea Accumulating evidence points to oxidative stress as an important factor in the onset of diabetic neuropathy. We have investigated the status of antioxidant protection mechanisms in immortalized rat Schwann cells cultured in high (30 and 50 mM) concentrations of glucose. As compared to growth in 5 mM glucose, the cells contained 40% less reduced glutathione (n =8, p < 0.01). Total superoxide dismutase activity was diminished by more than 50% (n=3; p < 0.001), whereas catalase activity was unchanged. The cellular NADH/NAD+ ratio was progressively increased with increasing medium glucose concentrations. Our previous findings have established that upon exposure of cultured cells to elevated glucose, the proportions of arachidonic acid-containing molecular species (ACMS) in phospholipids are decreased in a pattern similar to alterations exhibited by diabetic nerve. To examine whether biosynthesis of arachidonic acid might be perturbed, confluent cells maintained in either high or low glucose were incubated with either [14C]linoleic acid (18:2) or [14C]dihomo-,-linolenic acid (20:3) and radioactivity incorporated into molecular species of major phospholipid classes was measured. The incorporation of 18:2 either as unchanged fatty acid or into ACMS did not differ as a function of glucose concentration. Negligible labeled 18:3 or 20:3 molecular species were detected. In contrast, the uptake of 20:3 into 18:1/20:4 and 16:0/20:4 phosphatidylcholine and 18:1/20:4 phosphatidylethanolamine, but not into 20:3-containing molecular species, was significantly reduced in cells cultured in 30 mM glucose. These data imply that ,5 desaturase activity is decreased in cells exposed to elevated glucose. This reduced enzyme activity could adversely affect polyunsaturated fatty acid metabolism and might arise as a consequence of impaired scavenging of reactive oxygen species. (Supported by NIH grant DK30577) [source] Antioxidant and angiotension-converting enzyme inhibition capacities of various parts of Benincasa hispida (wax gourd)MOLECULAR NUTRITION & FOOD RESEARCH (FORMERLY NAHRUNG/FOOD), Issue 3 2004Hui-Yu Huang Abstract Vegetables and fruits have been shown to be good sources of antioxidants. Benincasa hispida (wax gourd) has been used in traditional Chinese medicine to treat hypertension and inflammation. The aims of this study were to investigate the abilities of antioxidation and inhibition of angiotensin-converting enzyme (ACE) activity of wax gourd pulp, core, seed, and peel prepared by different extraction methods. The fresh weights required to reach 50% inhibition of linoleic acid oxidation were higher in fresh extracts, compared to other extraction methods. Fresh weights required to reach 50% inhibition were the lowest in seed. The seed had the lowest Cu2+ -induced low-density lipoprotein (LDL) oxidation percentage and inhibition level of ACE activity among all parts. The higher antioxidant capacity of the seed may result from the higher total phenolics contents and superoxide dismutase activity. The abilities of antioxidation and ACE activity inhibition may provide protective effects against cardiovascular diseases and cancers. [source] Anti-inflammatory responses and oxidative stress in Nippostrongylus brasiliensis -induced pulmonary inflammationPARASITE IMMUNOLOGY, Issue 1 2002Kathryn S. McNeil summary Migration of L3 larvae of Nippostrongylus brasiliensis through the lungs of the rat, during primary infection, was studied at 24 h, 72 h and 8 days. At 24 h p.i., there was evidence of damage to lung epithelial cells and microvasculature, with increased protein and ,-glutamyl transpeptidase in the bronchoalveolar lavage (BAL) fluid. However, there was little evidence of inflammatory cell recruitment. At 24 h p.i., there was a significant reduction in the inflammatory cytokine tumour necrosis factor ,. Superoxide (O2,·) production was also reduced, accompanied by an increase in superoxide dismutase activity. Lipid peroxidation was reduced at 24 h p.i. and L3 larvae were shown to possess high levels of glutathione compared to host lung tissue. Nitric oxide, detected as nitrite, was produced in BAL fluid, and inducible nitric oxide synthase protein was increased by 72 h p.i. There was evidence of peroxynitrite production throughout the infection period with specific protein bands nitrosylated at 75, 30 and 25 kDa. It appears that despite early evidence of lung damage, the inflammation was reduced in response to L3 larvae of N. brasiliensis. [source] The effects of EGb 761 on lipid peroxide levels and superoxide dismutase activity in sunburnPHOTODERMATOLOGY, PHOTOIMMUNOLOGY & PHOTOMEDICINE, Issue 3 2002Mehtap Kilinc Ozkur Background/Purpose: Free oxygen radicals are involved in inflammatory skin reactions induced by ultraviolet B (UVB). In this study, the effect of a herbal antioxidant Ginkgo biloba extract (EGb 761) was investigated in UVB irradiated mice skin. Methods: The study was carried out on four groups of mice (n = 6 in each group). The first group was a control group (G1). The second group (G2) was only exposed to acute UVB irradiation. The third group (G3) received 100 mg/kg/day of EGb 761 orally for 5 days before UVB irradiation and the fourth group (G4) was given only a single dose of EGb 761 immediately after UVB irradiation. Eighteen hours after exposing to UVB, lipid peroxide levels, and superoxide dismutase (SOD) activities were studied and UVB damage was evaluated histopathologically according to ,sun-burn cell count'. Results: The SOD activities and Malondialdehyde (MDA) levels in G2, G3 and G4 were found to be decreased significantly when compared with G1 (P < 0.05). The SOD activities of G3 and G4 were higher when compared with G2 (P < 0.05). The number of sunburn cells (SBCs) was the highest in G2. Conclusions: Our results suggest that EGb 761 may have an important effect, both as a protective and therapeutic agent, in sunburn after UVB irradiation. [source] Prebiotics in aquaculture: a reviewAQUACULTURE NUTRITION, Issue 2 2010E. RINGŘ Abstract A prebiotic is a non-digestible food ingredient that beneficially affects the host by selectively stimulating the growth and/or the activity of one or a limited number of bacteria in the colon. Despite the potential benefits to health and performance as noted in various terrestrial animals, the use of prebiotics in the farming of fish and shellfish has been less investigated. The studies of prebiotics in fish and shellfish have investigated the following parameters: effect on growth, feed conversion, gut microbiota, cell damage/morphology, resistance against pathogenic bacteria and innate immune parameters such as alternative complement activity (ACH50), lysozyme activity, natural haemagglutination activity, respiratory burst, superoxide dismutase activity and phagocytic activity. This review discusses the results from these studies and the methods used. If the use of prebiotics leads to health responses becoming more clearly manifested in fish and shellfish, then prebiotics might have the potential to increase the efficiency and sustainability of aquaculture production. However, large gaps of knowledge exist. To fully conclude on the effects of adding prebiotics in fish diets, more research efforts are needed to provide the aquaculture industry, the scientific community, the regulatory bodies and the general public with the necessary information and tools. [source] Influence of several non-nutrient additives on nonspecific immunity and growth of juvenile turbot, Scophthalmus maximus L.AQUACULTURE NUTRITION, Issue 5 2008Y. LI Abstract The effects of three non-nutrient additives on nonspecific immunity and growth of juvenile turbot (Scophthalmus maximus L.) were studied in this feeding experiment. The five treatments are basal diet alone, basal diets containing three different additives [0.4 g kg,1 of xylo-oligosaccharides (XOS), 1.3 g kg ,1 of yeast cell wall and 0.8 g kg ,1 of bile acids] individually or in combination. Two hundred and twenty-five turbots (average initial weight 151.3 ± 11.3 g) were randomly allotted in five treatments with three replicates within each treatment in a 72-day period. Comparing with basal diet group, activities of C3, C4, phagocyte, lysozyme, specific growth rate and feed conversion rate in yeast cell wall, XOS and the combined groups was enhanced significantly (P < 0.05); however, these parameters in bile acid groups were increased slightly (P > 0.05) except for phagocyte (P < 0.05); superoxide dismutase activity in additive groups was not significantly increased (P > 0.05) except for the combined group (P < 0.05). In conclusion, supplementation of yeast cell wall and XOS enhanced the nonspecific immunity of juvenile turbot. Synergistic or additive effect of the three additives was not observed. [source] Regulation of autophagy in human and murine cartilage: Hypoxia-inducible factor 2 suppresses chondrocyte autophagyARTHRITIS & RHEUMATISM, Issue 5 2009Jolene Bohensky Objective We have previously demonstrated that the transcription factor hypoxia-inducible factor 1 (HIF-1) promotes the onset of autophagy in chondrocytes. The overall goal of this study was to test the hypothesis that another HIF family transcription factor, HIF-2, modulates the induction of autophagy by chondrocytes. Methods Expression of HIF-1, HIF-2, and light chain 3 (LC3) in human and murine articular cartilage was visualized by immunohistochemistry. Suppression of HIF-2 was achieved using small interfering RNA technology. Assessments of autophagic flux and lysosomal activity, as well as ultrastructural analysis, were performed in chondrocytes in cell culture. Results HIF-2 was expressed abundantly by cells in human and murine articular cartilage and in the cartilage of mineralizing vertebrae from neonatal mice. Protein levels were reduced in articular cartilage from older mice, in end-plate cartilage from mice, and in chondrocytes from human osteoarthritic (OA) cartilage. HIF-2 was robustly expressed in the prehypertrophic cells of mouse growth cartilage. When HIF-2, was silenced, the generation of reactive oxygen species was found to be elevated, with a concomitant decrease in catalase and superoxide dismutase activity. Suppression of HIF-2 was associated with decreased Akt-1 and mammalian target of rapamycin activities, reduced Bcl-xL expression, and a robust autophagic response, even under nutrient-replete conditions. In these silenced chondrocytes, HIF-1 expression was elevated. Decreased HIF-2 expression was associated with autophagy in OA tissues and aging cartilage samples. The autophagic response of chondrocytes in HIF-2,,knockout mouse growth plate showed an elevated autophagic response throughout the plate. Conclusion Based on these observations, we conclude that HIF-2 is a potent regulator of autophagy in maturing chondrocytes. Our data suggest that this protein acts as a brake on the autophagy-accelerator function of HIF-1. [source] Delayed Protection of Tetramethylpyrazine on Neonatal Rat Cardiomyocytes Subjected to Anoxia-Reoxygenation InjuryBASIC AND CLINICAL PHARMACOLOGY & TOXICOLOGY, Issue 6 2007He-Ping Chen Cultured neonatal rat cardiomyocytes were preconditioned using TMP at different concentrations (100, 200 and 500 µM). Cell viability, lactate dehydrogenase release, malondialdehyde formation, superoxide dismutase activity and glutathione peroxidase activity were measured to determine the protective effects against anoxia-reoxygenation injury. The expression of heat shock protein 70 (Hsp70) was measured 24 hr after TMP preconditioning by Western blot analysis. The results showed that TMP decreased lactate dehydrogenase release, increased cell viability, suppressed malondialdehyde formation and augmented activities of superoxide dismutase and glutathione peroxidase in a concentration-dependent manner. Moreover, the delayed protection was abolished by pre-treating with either protein kinase C inhibitor chelerythrine chloride or PD98059, a selective inhibitor of extracellular signal-regulated protein kinase 1/2, respectively, and the expression of Hsp70 was significantly increased in 24 hr after TMP preconditioning that was also suppressed by chelerythrine chloride or PD98059. These results suggest that TMP can induce delayed cardioprotective effects by activation of protein kinase C and extracellular signal-regulated protein kinase 1/2 signalling pathways and subsequent increased expression of Hsp70 in rat neonatal cardiomyocytes. [source] PROTECTIVE EFFECTS OF ICARIIN ON COGNITIVE DEFICITS INDUCED BY CHRONIC CEREBRAL HYPOPERFUSION IN RATSCLINICAL AND EXPERIMENTAL PHARMACOLOGY AND PHYSIOLOGY, Issue 8 2009Rui-Xia Xu SUMMARY 1Icariin is a major constituent of flavonoids derived from the Chinese medicinal herb Epimedium revicornum Maxim. The aim of the present study was to investigate whether icariin has protective effects on learning ability and memory in a rat model of chronic cerebral hypoperfusion. 2Chronic cerebral hypoperfusion was induced by permanent ligation of the common carotid artery in Wistar rats for 4 months. One month after permanent artery occlusion, rats were adminitered icariin at doses of 0, 30, 60 or 120 mg/kg per day, p.o., for 3 months. Neurobehavioural and neurobiochemical parameters were examined to evaluate the effects of icariin on cognitive deficits induced by chronic cerebral hypoperfusion. 3The Morris water maze test revealed that learning ability and memory were severely impaired in untreated rats, but were significantly improved in icariin-treated rats. Icariin treatment also ameliorated chronic cerebral hypoperfusion-induced oxidative stress in the brain, as evidenced by reduced malondialdehyde formation and maintained superoxide dismutase activity. In addition, the decreased hippocampal levels of acetylcholine, acetylcholinesterase and choline acetyltransferase associated with chronic cerebral hypoperfusion were significantly prevented by icariin treatment. 4In conclusion, icariin protects against cognitive deficits induced by chronic cerebral hypoperfusion in rats. These effects appear to be mediated through its anti-oxidant effects, as well as its effects on the circulatory and cholinergic systems. [source] Superoxide radical generation and Mn- and Cu-Zn superoxide dismutases activities in human leukemic cellsHEMATOLOGICAL ONCOLOGY, Issue 1 2003Masahiko Kato Abstract Mn- and Cu-Zn superoxide dismutase (SOD) activities and generation of superoxide radicals (O) were assessed in leukemic cells from 10 patients with acute myeloid or monocytic leukemia (AML) and 10 patients with acute lymphoblastic leukemia (ALL), using a sensitive, specific chemiluminescence method. Leukemic cells were classified according to the French,American,British classification. M4 AML cells from two patients produced some O upon stimulation with opsonized zymosan (OZ), phorbol myristate acetate (PMA) or N-formyl-methionyl-leucyl-phenylalanine (FMLP), but less than normal granulocytes or monocytes. M5b AML cells from one patient produced as much O in response to these stimulants as normal monocytes. No O generation was induced in other types of leukemic cells. Total SOD activity in AML cells was significantly greater in normal granulocytes, but was only half of the activity in ALL cells. Mn-SOD in AML cells was very low or undetectable. These results suggest that except in M5b cells, decreased O production may contribute to susceptibility to infections in AML patients. Decreased Mn-SOD activity in AML cells may predispose them to oxidative stress. Copyright © 2002 John Wiley & Sons, Ltd. [source] | ||||||||||||||||||||||||||||