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  • 1
    Electronic Resource
    Electronic Resource
    Neuromelanogenic and Cytotoxic Properties of Canine Brainstem Peroxidase (1987)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 48 (1987), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: We have isolated a heme protein from canine midbrains that possesses potent peroxidase activity. This enzyme catalyzes the oxidation of dopamine to neuromela-nin in the presence of H2O2. We have further shown that the isolated peroxidase possesses potent cytotoxic activity in the presence of superoxide or H2O2 and Cl−. The enzyme possesses an endogenous NAD(P)H oxidase activity that can promote the cytotoxic activity by virtue of its production of superoxide. Other enzymes such as dihydroorotate dehydrogenase and galactose oxidase, which produce O2−and H2O2, respectively, are also effective in promoting the cytotoxic activity of the brainstem peroxidase. Although rat erythrocytes were routinely used as the target cell, other cell types, including rat hepatoma and mouse neuroblastoma cells, are also susceptible to the toxic action of the peroxidase. The cytotoxic action of the brainstem peroxidase is dramatically enhanced by kainic acid and is significantly enhanced by Mn2+, whereas dopamine was found to be a potent inhibitor of the cytotoxic activity. Based on these findings, we postulate a central role for the brainstem peroxidase in dopamine metabolism as well as in the biochemical and anatomical changes associated with Parkinson's disease.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1471-4159.1987.tb05598.x
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  • 2
    Electronic Resource
    Electronic Resource
    Role of NADPH oxidase in the brain injury of intracerebral hemorrhage (2005)
    Oxford, UK : Blackwell Science Ltd
    Journal of neurochemistry 94 (2005), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: The major risk factors for intracerebral hemorrhage (ICH) are hypertension and aging. A fundamental mechanism for hypertension- and aging-induced vascular injury is oxidative stress. We hypothesize that oxidative stress has a crucial role in ICH. To test our hypothesis, we used bacterial collagenase to produce ICH in wild-type C57BL/6 and gp91phox knockout (gp91phox KO) mice (deficient in gp91phox subunit of the superoxide-producing enzyme NADPH oxidase). All animals were studied at 20–35 weeks of age, resembling an older patient population. We found that collagenase produced less bleeding in gp91phox KO mice than wild-type mice. Total oxidative product was lower in gp91phox KO mice than in wild-type mice, both under basal conditions and after ICH. Consistent with the ICH volume, brain edema formation, neurological deficit and a high mortality rate was noted in wild-type but not in gp91phox KO mice. This ICH-induced brain injury in wild-type mice is associated with enhanced expression of the gp91phox subunit of NADPH oxidase. In conclusion, the oxidative stress resulting from activation of NADPH oxidase contributes to ICH induced by collagenase and promotes brain injury.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1471-4159.2005.03292.x
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  • 3
    Electronic Resource
    Electronic Resource
    Neutrophils, Nitrogen Oxides, and Inflammatory Bowel Disease (1992)
    Oxford, UK : Blackwell Publishing Ltd
    Annals of the New York Academy of Sciences 664 (1992), S. 0 
    Details
    ISSN: 1749-6632
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Natural Sciences in General
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1749-6632.1992.tb39753.x
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  • 4
    Electronic Resource
    Electronic Resource
    Myeloperoxidase-catalyzed incorporation of amines into proteins: role of hypochlorous acid and dichloramines (1982)
    s.l. : American Chemical Society
    Biochemistry 21 (1982), S. 6299-6308 
    Details
    ISSN: 1520-4995
    Source: ACS Legacy Archives
    Topics: Biology , Chemistry and Pharmacology
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1021/bi00267a040
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  • 5
    Electronic Resource
    Electronic Resource
    5-Aminosalicylic acid concentration in mucosal interstitium of cat small and large intestine (1989)
    Springer
    Digestive diseases and sciences 34 (1989), S. 573-578 
    Details
    ISSN: 1573-2568
    Keywords: ulcerative colitis ; sulfasalazine ; inflammation ; intestinal transport
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Uncertainty regarding the concentration of 5-ASA within the mucosal interstitium has been a major limitation of defining the protective mechanisms of 5-ASA in intestinal inflammation. Therefore, we measured the concentration of 5-ASA in intestinal lymph and venous plasma during luminal perfusion of the cat small and large intestine with 10 mM 5-ASA. Blood and lymph flows were measured in each segment. 5-ASA and N-acetyl-5-ASA were extracted from plasma and lymph and quantified using fluorescence spectroscopy. Luminal perfusion of the terminal ileum with 5-ASA resulted in the following concentration profile: intestinal venous plasma (143±30 μg/ml) ≫ lymph (43 ±17 μg/ml)=systemic arterial plasma (40±11 μg/ml). In the colon the local venous plasma concentration of 5-ASA was 20±6 μg/ml compared to 2.0±1.0 μg/ml in systemic arterial plasma. N-Acetyl-5-ASA was found to comprise less than 5% of the total metabolite concentration in both ileum and colon. We also found that 58% of luminal 5-ASA was absorbed per minute in the terminal ileum, whereas only 3%/min was absorbed from the colon. The results of this study suggest that: (1) the mucosal interstitial concentration of 5-ASA in the terminal ileum and colon are approximately 100 μg/ml (654 μM) and 20 μg/ml (164 μM), respectively; and (2) the rate of 5-ASA absorption in the terminal ileum is approximately seven times greater than that in the colon.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01536335
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  • 6
    Electronic Resource
    Electronic Resource
    Role of neutrophils in acetic acid-induced colitis in rats (1991)
    Springer
    Inflammation 15 (1991), S. 399-411 
    Details
    ISSN: 1573-2576
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Intrarectal administration of 4% acetic acid produces diffuse inflammation that ultimately results in erosions and ulcerations of the rat colon. Although this model of colitis has been used extensively over the past several years, there are no quantitative data available regarding the relationship between neutrophil infiltration and mucosal injury during times of active inflammation. Therefore, the objective of this study was to define the role of extravasated neutrophils as mediators of mucosal injury and inflammation in acetic acid-induced colitis. We found the intrarectal administration of 4% acetic acid produced an 11-fold increase in colonic mucosal permeability, a 9-fold increase in colonic MPO activity, and a 1.6-fold increase in colon weight at 48 h following administration of acetic acid. In addition, we found significant correlations between colonic MPO activity and mucosal permeability and between colonic MPO activity and colon weight (P 〈 0.01 for both). These data suggested that inflammatory neutrophils may mediate mucosal injury and inflammation in this model of colitis. To assess the role of circulating neutrophils, rats were rendered neutropenic for 48 h by the intraperitoneal administration of antiserum directed toward rat neutrophils (ANS). Although ANS treatment reduced both the number of circulating neutrophils and colonic MPO activity to less than 10% of control values, it did not attenuate the increases in colonic mucosal permeability nor did it attenuate the increases in colon weight produced by acetic acid. Histological inspection confirmed that ANS treatment was not effective in attenuating the injury to the epithelial barrier. These data demonstrate that infiltrating neutrophils do not mediate the mucosal injury and inflammation observed in acetic acid-induced colitis.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00917356
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  • 7
    Electronic Resource
    Electronic Resource
    Mechanisms of acute and chronic intestinal inflammation induced by indomethacin (1993)
    Springer
    Inflammation 17 (1993), S. 641-662 
    Details
    ISSN: 1573-2576
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The objective of this study was to characterize the mechanisms of acute and chronic intestinal mucosal injury and inflammation induced by subcutaneously injected indomethacin (Indo). One injection of Indo (7.5 mg/kg) produced acute injury and inflammation in the distal jejunum and proximal ileum that were maximal at three days and completely resolved within one week. Two daily subcutaneous injections of Indo produced a more extensive and chronic inflammation that lasted in an active form in more than 75% of the rats for at least two weeks. Epithelial injury, as measured by enhanced mucosal permeability, was significantly elevated only at one day in the acute model (one injection) but was persistently elevated in the chronic model (two injections). Bile duct ligation completely attenuated increased mucosal permeability in the acute model, however, depletion of circulating neutrophils had no effect. Neither Indo (0–0.1 mg/ml) nor normal bile was cytotoxic to cultured rat intestinal epithelial cells; however, they synergistically promoted significant cytotoxicity. Bile collected from rats treated with Indo was cytotoxic towards the epithelial cells in a dose-dependent manner. Sulfasalazine and metronidazole (100 mg/kg/day, both) attenuated enhanced mucosal permeability in the chronic model. Massive bacterial translocation into the mesenteric lymph nodes, liver, and spleen following two injections of Indo was significantly attenuated by metronidazole. We conclude that: (1) a single injection of Indo produces acute intestinal mucosal injury and inflammation that resolve completely within three to seven days, whereas two daily injections of Indo produce both acute and chronic injury and inflammation, (2) enterohepatic circulation of Indo is important in promoting the acute phases of injury and inflammation, (3) circulating neutrophils do not play a role in the pathogenesis of this model, and (4) endogenous bacteria play an important role in exacerbating and/or perpetuating the chronic phases of injury and inflammation.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00920471
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  • 8
    Electronic Resource
    Electronic Resource
    Inhibition of rat pleural mesothelial cell nitric oxide synthesis by transforming growth factor-β1 (1996)
    Springer
    Inflammation 20 (1996), S. 637-646 
    Details
    ISSN: 1573-2576
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Pleuritis is a common initial clinical manifestation of tuberculosis. It is associated with an accumulation of a variety of cytokines in the pleura and pleural fluid. We have recently shown that these proinflammatory cytokines induce the pleural mesothelial cell to produce large amounts of nitric oxide, a nitrogen intermediate that has been shown to have a tuberculocidal effect. TGF-β has also been found in situ in tuberculous effusions and pleural tissues and is thought to suppress the immune response and promote tissue repair. This study examined the effects of TGF-β on cytokine-induced NO synthesis by rat pleural mesothelial cells in vitro. Results demonstrated that TGF-β significantly inhibited NO synthesis and that this inhibition was associated with a proportionate decrease in iNOS mRNA and iNOS protein. Suppression of pleural mesothelial cell NO synthesis by TGF-β may be important in the pathogenesis of tuberculous pleuritis.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01488801
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  • 9
    Electronic Resource
    Electronic Resource
    Cytokines increase proliferation of human intestinal smooth muscle cells: Possible role in inflammation-induced stricture formation (1993)
    Springer
    Inflammation 17 (1993), S. 481-487 
    Details
    ISSN: 1573-2576
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Crohn's disease is an idiopathic, chronic inflammation of the gastrointestinal tract that causes narrowing and stricturing of primarily the small and large intestine. Although the mechanism(s) by which chronic inflammation promotes stricture formation remain to be defined, it does appear to be associated histologically with a hyperplasia of smooth muscle cells and an increased deposition of collagen within the bowel wall. The objective of this study was to assess the effect of two proinflammatory cytokines, tumor necrosis factor and interleukin-1, on the proliferation of human intestinal smooth muscle cells in vitro. Human intestinal smooth muscle cells were seeded at subconfluent densities into 24-well plates in Dulbecco's modified Eagle's medium supplemented with 10% fetal bovine serum. Human recombinant tumor necrosis factor (0.1–100 ng/ml), interleukin-1 (0.1–500 ng/ml), or control medium (without cytokines) was then added to the cells and incubation continued for 48 or 72 h. Proliferation was determined by the incorporation of tritiated thymidine, added during the final 18 h, into the cellular DNA of the smooth muscle cells. Both cytokines caused a significant dose-dependent increase in intestinal smooth muscle cell proliferation relative to control. These results suggest that the interleukin-1 and tumor necrosis factor produced during chronic inflammation in vivo may enhance the proliferation of smooth muscle cells within the intestinal bowel wall and hence potentially contribute to the narrowing and stricturing of the intestine that is observed in Crohn's disease.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00916587
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  • 10
    Electronic Resource
    Electronic Resource
    Prooxidant properties of 5-aminosalicylic acid (1992)
    Springer
    Digestive diseases and sciences 37 (1992), S. 1383-1389 
    Details
    ISSN: 1573-2568
    Keywords: pancreatitis ; iron ; free radicals ; hydrogen peroxide ; lipid peroxidation
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract There is a growing body of experimental and clinical evidence to suggest that oral or rectal administration of 5-ASA or 5-ASA conjugates is associated with significant adverse side effects including pancreatitis, hepatitis, and renal toxicity. The objective of this study was to assess the ability of 5-ASA to interact with low-molecular-weight iron to yield oxygen-derived free radicals and to determine whether these oxidants could damage model biological compounds. We found that 5-ASA was very effective at chelating ferric iron (Fe3+), and it rapidly reduced Fe3+ to the ferrous form (Fe2+). Addition of the 5-ASA/Fe2+ chelate to solutions containing polyunsaturated fatty acids or deoxyribose resulted in lipid peroxidation and oxidative carbohydrate degradation, respectively. These results are consistent with the formation of the highly reactive (and cytotoxic) hydroxyl radical. Formation of this free radical species was confirmed by the ability of hydroxyl radical scavengers (dimethyl sulfoxide, dimethyl thiourea) to inhibit the 5-ASA/Femediated oxidative reactions. Maximum hydroxyl radical formation was achieved at a 5-ASA-to-Fe3+ ratio of 1.0 (20 μM 5-ASA and 20 μM Fe3+). Increasing this ratio significantly inhibited OH·formation with a concomitant reduction in lipid peroxidation and deoxyribose degradation. Finally, we demonstrated that 5-ASA promotes the reductive release of Fe3+ from ferritin. Data obtained in this study suggest that 5-ASA may, under certain conditions, promote the formation of potentially injurious free radical species. These oxidative reactions may contribute to some of the adverse side effects known to be associated with the newer preparations of 5-ASA.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01296008
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