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Lawrence D Horwitz - One of the best experts on this subject based on the ideXlab platform.
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reduction of canine myocardial infarct size by a diffusible Reactive Oxygen Metabolite scavenger efficacy of dimethylthiourea given at the onset of reperfusion
Circulation Research, 1991Co-Authors: Frank P Carrea, Edward J Lesnefsky, John E Repine, R H Shikes, Lawrence D HorwitzAbstract:A number of scavengers of Reactive Oxygen Metabolites reduce myocardial injury when given before ischemia and reperfusion, but few, if any, have proven to be effective when given near the onset of reperfusion. This is particularly true when infarct size is measured after at least 48 hours of reperfusion, when the full extent of myocardial damage has become apparent. Dimethylthiourea (DMTU) is an extremely diffusible, potent scavenger of hydroxyl radical, hydrogen peroxide, and hypochlorous acid, with a long half-life of 43 hours. Sixteen chloralose-anesthetized dogs underwent 90 minutes of left anterior descending coronary artery (LAD) occlusion followed by 48 hours of reperfusion. Collateral flow was measured by radioactive microspheres. Infarct size and risk area were measured by a postmortem dual-perfusion technique using triphenyl tetrazolium chloride and Evan's blue dye. In eight dogs, therapy with DMTU (500 mg/kg i.v.) was given during the last 15 minutes of ischemia and the first 15 minutes of reperfusion. In eight control dogs, the same volume of 0.9% saline was given during the last 15 minutes of ischemia through the first 15 minutes of reperfusion. Infarct size as a percent of risk area was reduced in the DMTU-treated group compared with the saline-treated controls (DMTU = 42 +/- 4% versus saline = 59 +/- 4%, p less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)
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reduction of canine myocardial infarct size by a diffusible Reactive Oxygen Metabolite scavenger efficacy of dimethylthiourea given at the onset of reperfusion
Circulation Research, 1991Co-Authors: Frank P Carrea, Edward J Lesnefsky, John E Repine, R H Shikes, Lawrence D HorwitzAbstract:A number of scavengers of Reactive Oxygen Metabolites reduce myocardial injury when given before ischemia and reperfusion, but few, if any, have proven to be effective when given near the onset of reperfusion. This is particularly true when infarct size is measured after at least 48 hours of reperfusion, when the full extent of myocardial damage has become apparent. Dimethylthiourea (DMTU) is an extremely diffusible, potent scavenger of hydroxyl radical, hydrogen peroxide, and hypochlorous acid, with a long half-life of 43 hours. Sixteen chloralose-anesthetized dogs underwent 90 minutes of left anterior descending coronary artery (LAD) occlusion followed by 48 hours of reperfusion. Collateral flow was measured by radioactive microspheres. Infarct size and risk area were measured by a postmortem dual-perfusion technique using triphenyl tetrazolium chloride and Evan's blue dye. In eight dogs, therapy with DMTU (500 mg/kg i.v.) was given during the last 15 minutes of ischemia and the first 15 minutes of repe...
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Reactive Oxygen Metabolite scavengers decrease functional coronary microvascular injury due to ischemia reperfusion
American Journal of Physiology-heart and Circulatory Physiology, 1991Co-Authors: Ira M Dauber, Edward J Lesnefsky, Karyl M Vanbenthuysen, J V Weil, Lawrence D HorwitzAbstract:The role of Reactive Oxygen Metabolites in ischemia-reperfusion coronary microvascular injury is unclear. To investigate this problem, we tested the effects of the Reactive Oxygen Metabolite scavengers superoxide dismutase (SOD) and dimethylthiourea (DMTU) on ischemia-reperfusion-induced coronary microvascular dysfunction. As an index of vascular function, we assessed microvascular permeability with a double radioisotope protein leak index (PLI) method. Anesthetized dogs underwent 60 min of ischemia via left anterior descending (LAD) occlusion followed by 60 min of reperfusion. Untreated animals (n = 7) received saline. SOD-treated animals (n = 6) received 140 U.kg-1.min-1 (6.6 mg.kg-1.min-1) bovine SOD throughout ischemia and reperfusion. DMTU-treated animals (n = 5) received a 500 mg/kg bolus 30 min before ischemia. At the beginning of reperfusion, radiolabeled autologous protein (113mIn transferrin) and red blood cells (99mTc) were given intravenously for the assessment of permeability. In untreated dogs, ischemia-reperfusion increased the PLI of ischemic (flow less than 20 ml.min-1.100 g-1) myocardium more than threefold compared with that of nonischemic (flow greater than 100 ml.min-1.100 g-1) myocardium (ischemic-to-nonischemic PLI ratio = 3.49 +/- 0.48). SOD reduced the PLI of ischemic myocardium by 45% and DMTU reduced it by 66% (PLI = 9.25 +/- 1.30, 5.04 +/- 1.18, and 3.16 +/- 0.94, untreated, SOD, and DMTU, respectively). The PLI was increased proportional to the regional severity of ischemic blood flow. Both SOD and DMTU reduced the increase in protein leak at all levels of regional ischemic blood flow. Neither SOD nor DMTU increased regional myocardial blood flow to the occluded LAD zone.(ABSTRACT TRUNCATED AT 250 WORDS)
Eiji Yano - One of the best experts on this subject based on the ideXlab platform.
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Reactive Oxygen Metabolite production induced by asbestos and glass fibers effect of fiber milling
Industrial Health, 2003Co-Authors: Toyoto Iwata, Eiji YanoAbstract:Particle stimulated chemiluminescence (CL) production by human polymorphonuclear leucocytes (PMN) has been utilized to evaluate the pathogenicity of mineral and glass fibers with the understanding that Reactive Oxygen Metabolites (ROM) production as measured by CL is etiopathogenically related to fiber toxicity. In the present study to investigate the specific pathogenic role of fiber number and dimensions, CL production from PMN exposed to anthophyllite asbestos mineral and glass fiber samples milled for different time periods was measured. Almost all the fibrous particles in the glass fiber sample were destroyed after milling for 30 minutes. With anthophyllite, the total number of fibrous particles remained almost constant for up to 240 minutes of milling, although the size of fibrous particles was reduced. CL produced by the same mass of glass fiber was elevated after milling for 15 minutes, but then declined when the milling time was further increased. Similarly, with anthophyllite, the production of CL was elevated at the first period of milling for 30 minutes, but then declined at the longer milling times. The level of CL produced was not correlated to the total number of fibrous particles, for both the glass fiber and the anthophyllite samples. Likewise for the glass fiber and anthophyllite samples, no specific range of fiber dimension was correlated to the peak hight CL production. These findings indicate that neither the total number, nor the specific range of fiber dimension solely determines CL production. As a consequence, it may be concluded that other physiochemical factors, such as the surface Reactive characteristics of milled fibers, may be more closely related to CL production by PMN.
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chemiluminescent detection of induced Reactive Oxygen Metabolite production of human polymorphonuclear leucocytes by anthophyllite asbestos
Environmental Research, 2002Co-Authors: Toyoto Iwata, Norihiko Kohyama, Eiji YanoAbstract:Incidences of lung cancer and pleural plaque have been reported in relation to exposure to anthophyllite asbestos. To investigate the pathogenic mechanisms of anthophyllite, chemiluminescence (CL) detection of Reactive Oxygen Metabolite (ROM) generation of human polymorphonuclear leucocytes (PMN) stimulated by anthophyllite asbestos was determined and compared with that of other asbestos and mineral fiber samples. When anthophyllite fiber sample was mixed with the luminol-primed PMN, high levels of CL which exhibited a specific time course characterized by two separate peaks were induced. The CL induced by anthophyllite sample was greater than that induced by chrysotile, crocidolite, and amosite asbestos. We further investigated the two peaks of CL using specific inhibitors of signal transduction mechanisms. The two peaks of CL by anthophyllite sample were different in sensitivity to cytochalasin B and genistein; the former relates to the cytoskeleton-dependent mechanism and the latter has been shown to inhibit tyrosine kinase, which resides in the pathway to cause PMN activation. The strong ROM reaction of PMN by anthophyllite suggests that the surface characteristics of the fiber may participate in the pathogenic mechanisms of anthophyllite asbestos.
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Cellular mechanisms of Reactive Oxygen Metabolite generation from human polymorphonuclear leukocytes induced by crocidolite asbestos.
Environmental Research, 1997Co-Authors: Tatsuro Ishizaki, Eiji Yano, Peterh. EvansAbstract:In our previous study, we demonstrated that Reactive Oxygen Metabolites (ROM) generation from phagocytic cells may be involved in the carcinogenic mechanism of crocidolite asbestos. In the present study, the mechanism of human polymorphonuclear leukocytes (PMN) to generate ROM by crocidolite was investigated using verapamil, a calcium channel inhibitor; staurosporine, a NADPH oxidase inhibitor; and cytochalasin B (CB), an inhibitor of phagocytosis. The results indicate that whereas verapamil and staurosporine inhibited the crocidolite-induced ROM generation from PMN dose-dependently, CB caused an enhancement. We conclude that crocidolite-induced ROM generation involves a cell surface reaction due to influx of extracellular calcium through calcium channels and the activation of NADPH oxidase on the PMN cell membrane. This hypothesis was indirectly supported by dose-dependent enhancement of the ROM generation by CB, as CB increases calcium ion permeability in PMN. However, as in our previous studies, the time course of the ROM generation and the cell type difference suggested that ROM were also generated intracellularly from PMN due to phagocytosis of crocidolite. In conclusion, our evidence indicates that ROM generation from PMN by crocidolite involves cellular mechanisms related both to direct cell surface membrane interactions, together with an apparent phagocytic-dependent process.
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Reactive Oxygen Metabolite production induced by mineral fibres
1991Co-Authors: Eiji Yano, Naoko Urano, P H EvansAbstract:Recently, increasing attention has been devoted to the role of Reactive Oxygen Metabolites (ROM) in the pathogenic mechanism of various carcinogens. For example, chemical carcinogens such as benzo-(a)-pyrene, 4-nitroquinoline-N-oxide and naphthylamines have been shown to produce free radicals in biologic systems, and the carcinogenicity of these chemicals have been related to such interactions. Carcinogenicity of ionising radiation which had been believed to cause direct modification of DNA strands, is now attributed to the interactions with hydroxyl radical (OH •) produced from cytosolic water.
D S Rampton - One of the best experts on this subject based on the ideXlab platform.
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relationship between infective load of helicobacter pylori and Reactive Oxygen Metabolite production in antral mucosa
Scandinavian Journal of Gastroenterology, 1994Co-Authors: G R Davies, Nicholas Banatvala, C E Collins, M T Sheaff, Y Abdi, L Clements, D S RamptonAbstract:Davies GR, Banatvala N, Collins CE, Sheaff MT, Abdi Y, Clements L, Rampton DS. Relationship between infective load of Helicobacter pylori and Reactive Oxygen Metabolite production in antral mucosa. Scand J Gastroenterol 1994;29:419-424.Helicobacter pylori infection has been associated with stimulation of gastric mucosal Reactive Oxygen Metabolite production. To provide further evidence of a causal relationship we looked for a dose-response relationship. We studied antral biopsy material from 110 patients. Quantitative H. pylori assessments were made using histologic and microbiologic methods. Reactive Oxygen Metabolite production was measured by luminol-dependent chemiluminescence. The usefulness of timed urease test colour changes as a guide to infective load was assessed. There was a positive association between mucosal Reactive Oxygen Metabolite production and histologic (p = 0.002, n = 69) and microbiologic (Spearman's R = + 0.6, p = 0.05, n = 18) quantitative H. pylori assessments. H. pylori infectiv...
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helicobacter pylori stimulates antral mucosal Reactive Oxygen Metabolite production in vivo
Gut, 1994Co-Authors: G R Davies, Nicholas Banatvala, M T Sheaff, N J Simmonds, T R J Stevens, I F Laurenson, D R Blake, D S RamptonAbstract:To determine if Reactive Oxygen Metabolites have a pathogenic role in Helicobacter pylori (H pylori) related gastroduodenal disease, this study measured their production in antral mucosal biopsy specimens. Two related chemiluminescence techniques were used comparing H pylori positive (n = 105) and negative patients (n = 64) with a similar spectrum of macroscopic disease. After chemiluminescence assays, biopsy specimens were graded histologically. Increased luminol dependent chemiluminescence (detecting Reactive Oxygen Metabolites through peroxidase catalysed reactions) was found in H pylori positive patients (median photon emission = 6.4 x 10(3)/min/mg wet weight (95% confidence intervals 3.6 to 9.9)) but not H pylori negative cases (-0.9 (-1.3 to -0.6)) (p = 0.0001). Similar results were found using lucigenin (which reacts directly with Oxygen Metabolites, particularly superoxide): (H pylori positive 0.9 (0.1 to 3.2); H pylori negative -1.2 (-3.4 to -0.6)) (p = 0.0003). Chemiluminescence was greater in H pylori positive compared with negative tissue when samples were grouped by equivalent macroscopic or microscopic damage. This difference was in part accounted for by a greater neutrophil infiltration in the H pylori positive mucosa, but when biopsy specimens with equivalent neutrophil infiltration could be compared directly, positive specimens gave greater chemiluminescence than negative. Smoking, drugs, and alcohol consumption had no independent effect. It is concluded that excess mucosal Reactive Oxygen Metabolite production is associated with H pylori gastric antral infection and may be an important pathogenic mechanism. There is no evidence for Reactive Oxygen Metabolite participation in the pathogenesis of gastric mucosal injury in cases unrelated to H pylori infection.
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mucosal Reactive Oxygen Metabolite production in duodenal ulcer disease
Gut, 1992Co-Authors: G R Davies, N J Simmonds, T R J Stevens, D R Blake, A Grandison, D S RamptonAbstract:To investigate the hypothesis that Reactive Oxygen Metabolites are important in the pathophysiology of duodenal ulcer disease, their production by duodenal mucosal biopsy specimens was measured using luminol and lucigenin amplified chemiluminescence. Luminol chemiluminescence, expressed as background corrected median photon emission/mg/min x 10(3) (95% confidence intervals), was increased in duodenal inflammation as assessed macroscopically: ulcers 20.3 (4.8 to 51.3), n = 29; severe duodenitis 13.9 (6.6 to 75.3), n = 16; mild duodenitis 0.0 (-0.5 to 0.8), n = 56; controls -0.8 (-1.3 to -0.1), n = 41; p = 0.0001, Kruskal-Wallis) and microscopically: severe 17.0 (9.3 to 51.3), n = 12; moderate 0.3 (-2.8 to 5.8), n = 17; mild -0.1 (-1.8 to 1.0), n = 17; controls -0.8 (-1.6 to 0.0), n = 15; (p = 0.0001). Luminol chemiluminescence was directly related to both the macroscopic and microscopic severity of duodenal damage (Spearman's R = + 0.53, + 0.55 respectively, both p = 0.0001), to histochemical assessment (myeloperoxidase activity) of neutrophil infiltration (R = + 0.63; p = 0.04), and to lucigenin chemiluminescence (R = + 0.56, p = 0.0002). Luminol chemiluminescence was inhibited by sodium azide (-80%), catalase (-73%), and dimethyl sulphoxide (-24%). Superoxide dismutase inhibited lucigenin more than luminol dependent chemiluminescence (-61% and -7% respectively, p < 0.05). Within disease groups, Helicobacter pylori antral infection was associated with increased duodenal chemiluminescence, whereas smoking, alcohol, and use of NSAIDs or H2 blockers had no influence. Their disease related generation in duodenal mucosa supports a role for Reactive Oxygen Metabolites in the pathogenesis of duodenitis and duodenal ulcer. These Metabolites might include superoxide, hydrogen peroxide, hydroxyl, and products of myeloperoxidase activity.
G R Davies - One of the best experts on this subject based on the ideXlab platform.
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non steroidal anti inflammatory drugs inhibit helicobacter pylori induced human neutrophil Reactive Oxygen Metabolite production in vitro
Alimentary Pharmacology & Therapeutics, 1999Co-Authors: S Jonesblackett, G R Davies, Mark A Hull, Jean E CrabtreeAbstract:Background: Helicobacter pylori infection is associated with increased production of gastric mucosal Reactive Oxygen Metabolites which have been implicated in mucosal damage and carcinogenesis. In vitro, neutrophils produce Reactive Oxygen Metabolites following activation by H. pylori. Non-steroidal anti-inflammatory drugs (NSAIDs) inhibit neutrophil activation by several factors, e.g. N-formyl-methionyl-leucyl-phenyalanine (f-MLP). Aim: To examine the effect of NSAIDs on H. pylori-induced Reactive Oxygen Metabolite production by human peripheral blood neutrophils. Methods: Neutrophils were stimulated by H. pylori (NCTC 11637) water extract or f-MLP in the presence or absence of NSAIDs. Reactive Oxygen Metabolite activity was measured by luminol-enhanced chemiluminescence. Results: H. pylori water extract stimulated a sevenfold increase in chemiluminescence which was inhibited dose-dependently by diclofenac. All six NSAIDs studied (at 10–4 M) significantly inhibited H. pylori-and f-MLP-stimulated neutrophil Reactive Oxygen Metabolite production. Meclofenamic acid and diclofenac had the greatest inhibitory effects on both H. pylori and f-MLP-stimulated neutrophil Reactive Oxygen Metabolite production. The inhibitory effects of other NSAIDs varied with the activation stimulus. NSAIDs did not quench Reactive Oxygen Metabolites generated in a cell-free xanthine:xanthine oxidase assay. Conclusion: Several NSAIDs attenuate H. pylori-induced neutrophil Reactive Oxygen Metabolites production in vitro. This may be relevant to a potential chemopreventative role in gastric cancer and to a possible lack of synergy between H. pylori and NSAID use regarding peptic ulceration.
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relationship between infective load of helicobacter pylori and Reactive Oxygen Metabolite production in antral mucosa
Scandinavian Journal of Gastroenterology, 1994Co-Authors: G R Davies, Nicholas Banatvala, C E Collins, M T Sheaff, Y Abdi, L Clements, D S RamptonAbstract:Davies GR, Banatvala N, Collins CE, Sheaff MT, Abdi Y, Clements L, Rampton DS. Relationship between infective load of Helicobacter pylori and Reactive Oxygen Metabolite production in antral mucosa. Scand J Gastroenterol 1994;29:419-424.Helicobacter pylori infection has been associated with stimulation of gastric mucosal Reactive Oxygen Metabolite production. To provide further evidence of a causal relationship we looked for a dose-response relationship. We studied antral biopsy material from 110 patients. Quantitative H. pylori assessments were made using histologic and microbiologic methods. Reactive Oxygen Metabolite production was measured by luminol-dependent chemiluminescence. The usefulness of timed urease test colour changes as a guide to infective load was assessed. There was a positive association between mucosal Reactive Oxygen Metabolite production and histologic (p = 0.002, n = 69) and microbiologic (Spearman's R = + 0.6, p = 0.05, n = 18) quantitative H. pylori assessments. H. pylori infectiv...
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helicobacter pylori stimulates antral mucosal Reactive Oxygen Metabolite production in vivo
Gut, 1994Co-Authors: G R Davies, Nicholas Banatvala, M T Sheaff, N J Simmonds, T R J Stevens, I F Laurenson, D R Blake, D S RamptonAbstract:To determine if Reactive Oxygen Metabolites have a pathogenic role in Helicobacter pylori (H pylori) related gastroduodenal disease, this study measured their production in antral mucosal biopsy specimens. Two related chemiluminescence techniques were used comparing H pylori positive (n = 105) and negative patients (n = 64) with a similar spectrum of macroscopic disease. After chemiluminescence assays, biopsy specimens were graded histologically. Increased luminol dependent chemiluminescence (detecting Reactive Oxygen Metabolites through peroxidase catalysed reactions) was found in H pylori positive patients (median photon emission = 6.4 x 10(3)/min/mg wet weight (95% confidence intervals 3.6 to 9.9)) but not H pylori negative cases (-0.9 (-1.3 to -0.6)) (p = 0.0001). Similar results were found using lucigenin (which reacts directly with Oxygen Metabolites, particularly superoxide): (H pylori positive 0.9 (0.1 to 3.2); H pylori negative -1.2 (-3.4 to -0.6)) (p = 0.0003). Chemiluminescence was greater in H pylori positive compared with negative tissue when samples were grouped by equivalent macroscopic or microscopic damage. This difference was in part accounted for by a greater neutrophil infiltration in the H pylori positive mucosa, but when biopsy specimens with equivalent neutrophil infiltration could be compared directly, positive specimens gave greater chemiluminescence than negative. Smoking, drugs, and alcohol consumption had no independent effect. It is concluded that excess mucosal Reactive Oxygen Metabolite production is associated with H pylori gastric antral infection and may be an important pathogenic mechanism. There is no evidence for Reactive Oxygen Metabolite participation in the pathogenesis of gastric mucosal injury in cases unrelated to H pylori infection.
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mucosal Reactive Oxygen Metabolite production in duodenal ulcer disease
Gut, 1992Co-Authors: G R Davies, N J Simmonds, T R J Stevens, D R Blake, A Grandison, D S RamptonAbstract:To investigate the hypothesis that Reactive Oxygen Metabolites are important in the pathophysiology of duodenal ulcer disease, their production by duodenal mucosal biopsy specimens was measured using luminol and lucigenin amplified chemiluminescence. Luminol chemiluminescence, expressed as background corrected median photon emission/mg/min x 10(3) (95% confidence intervals), was increased in duodenal inflammation as assessed macroscopically: ulcers 20.3 (4.8 to 51.3), n = 29; severe duodenitis 13.9 (6.6 to 75.3), n = 16; mild duodenitis 0.0 (-0.5 to 0.8), n = 56; controls -0.8 (-1.3 to -0.1), n = 41; p = 0.0001, Kruskal-Wallis) and microscopically: severe 17.0 (9.3 to 51.3), n = 12; moderate 0.3 (-2.8 to 5.8), n = 17; mild -0.1 (-1.8 to 1.0), n = 17; controls -0.8 (-1.6 to 0.0), n = 15; (p = 0.0001). Luminol chemiluminescence was directly related to both the macroscopic and microscopic severity of duodenal damage (Spearman's R = + 0.53, + 0.55 respectively, both p = 0.0001), to histochemical assessment (myeloperoxidase activity) of neutrophil infiltration (R = + 0.63; p = 0.04), and to lucigenin chemiluminescence (R = + 0.56, p = 0.0002). Luminol chemiluminescence was inhibited by sodium azide (-80%), catalase (-73%), and dimethyl sulphoxide (-24%). Superoxide dismutase inhibited lucigenin more than luminol dependent chemiluminescence (-61% and -7% respectively, p < 0.05). Within disease groups, Helicobacter pylori antral infection was associated with increased duodenal chemiluminescence, whereas smoking, alcohol, and use of NSAIDs or H2 blockers had no influence. Their disease related generation in duodenal mucosa supports a role for Reactive Oxygen Metabolites in the pathogenesis of duodenitis and duodenal ulcer. These Metabolites might include superoxide, hydrogen peroxide, hydroxyl, and products of myeloperoxidase activity.
J Kevin M D Ivey - One of the best experts on this subject based on the ideXlab platform.
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role of cellular superoxide dismutase against Reactive Oxygen Metabolite induced cell damage in cultured rat hepatocytes
Hepatology, 1992Co-Authors: Yasuaki Ito, H Hiraishi, Mahnaz Razandi, Akira Terano, Takashi Harada, J Kevin M D IveyAbstract:Reactive Oxygen Metabolites have been reported to be important in the pathogenesis of ischemia/reperfusion-induced and alcohol-and druginduced liver injuries. We investigated the role of superoxide dismutase, cellular and extracellular, in preventing Reactive Oxygen Metabolite–induced cytotoxicity in cultured rat hepatocytes. Cells were exposed to Reactive Oxygen Metabolites enzymatically generated by hypoxanthine-xanthine oxidase. Cytotoxicity was quantified by measuring51Cr release from prelabeled cells and lactate dehydrogenase release. Reactive Oxygen Metabolites caused dose-dependent cytotoxicity. Good correlation was found between the values for51Cr and lactate dehydrogenase release. Reactive Oxygen Metabolite–induced cell damage was reduced by catalase but not by superoxide dismutase. Cellular superoxide dismutase and catalase activities were not increased after incubation with exogenous superoxide dismutase and catalase for up to 5 hr. Pretreatment with diethyldithiocarbamate inhibited cellular superoxide dismutase activity without inhibiting other antioxidants such as catalase, glutathione, glutathione reductase and glutathione peroxidase and sensitized cells to Reactive Oxygen Metabolite–induced cytotoxicity. We conclude that hydrogen peroxide is an important mediator in hypoxanthine-xanthine oxidase–induced cell damage and that superoxide dismutase plays a critical role in cellular antioxidant defenses against hypoxanthine-xanthine oxidase–induced cytotoxicity in cultured rat hepatocytes in vitro. (HEPATOLOGY 1992;16:247–254.)
