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  • 1
    Electronic Resource
    Electronic Resource
    The inhibition of silica-induced lung inflammation by dexamethasone as measured by bronchoalveolar lavage fluid parameters and peroxynitrite-dependent chemiluminescence (1994)
    Springer
    Inflammation research 41 (1994), S. 44-49 
    Details
    ISSN: 1420-908X
    Keywords: Silica ; Lung ; Inflammation ; Dexamethasone ; Peroxynitrite ; Chemiluminescence
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The inhalation of silica has been shown to produce a dramatic inflammatory and toxic response within the lungs of humans and laboratory animals. Currently, no effective treatment exists for workers who may have been exposed to the inhalation of silica. The objective of this study was to develop an animal model in which we could evaluate the effect that anti-inflammatory steroids have on the acute silica-induced pulmonary inflammatory response. Male Fischer 344 rats were pretreated with either dexamethasone (2 mg/kg) or saline vehicle (i.p.) on days 1, 3, and 5. On day 6, the animals from the two groups were then intratracheally instilled with either silica (20 mg/0.5 ml saline vehicle) or saline vehicle (0.5 ml). Twenty-four hours after the instillations in the non-steroid group, significant increases occurred in total protein, total number of cells, neutrophils, and lymphocytes recovered from the lungs of animals treated with silica compared to saline controls. Silica also caused dramatic increases in the luminol-dependent chemiluminescence (LDCL) of lung tissue and bronchoalveolar lavage (BAL) cells. The LDCL reaction was markedly decreased by either superoxide dismutase (SOD) orN-nitro-l-arginine methyl ester hydrochloride (l-NAME). SOD is involved in the enzymatic breakdown of superoxide anion, whilel-NAME, a nitric oxide (NO) synthase inhibitor, prevents the formation of NO. When the superoxide anion and NO react, they form the highly oxidizing substance peroxynitrite. This study then implicates peroxynitrite as an agent which may be involved in the silica-induced oxidant lung injury. When the animals were pretreated with the steroid dexamethasone, there was a complete protection against the biochemical, cellular, and chemiluminescent indices of damage caused by silica. The mechanism in which the steroid protects the lung from damage may be due to the ability of dexamethasone to block the induction of NO synthase. With further study in animals, the anti-inflammatory steroids may be useful in the treatment of silicainduced lung injury.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01986392
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  • 2
    Electronic Resource
    Electronic Resource
    Comparison of the effects of antioxidant non-steroidal anti-inflammatory drugs against myeloperoxidase and hypochlorous acid luminol-enhanced chemiluminescence (1982)
    Springer
    Inflammation research 12 (1982), S. 232-238 
    Details
    ISSN: 1420-908X
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The interaction of myeloperoxidase (MPO) with H2O2 and Cl− provides a potent antimicrobial/cytotoxic system for polymorphonuclear leukocytes (PMNs). MPO-related cytotoxicity may be associated with the formation of toxic oxidant MPO intermediates, HOCl, or both. MPO itself is able to oxidize drugs and cellular components. Non-steroidal anti-inflammatory drugs (NSAIDs) able to act as antioxidant free radical scavengers have recently been shown to inhibit luminol-enhanced chemiluminescence (CL) which results from the MPO−H2O2−Cl− reaction. CL is a measure of the activity of this reaction. At that time it was not clear whether the source of CL which these NSAIDs affected was HOCl or components of the initial MPO−H2O2−Cl− reaction. A NSAID antioxidant mechanism could affect MPO oxidant intermediates and HOCl. This study compares the effects of antioxidant NSAIDs, methylprednisone and free radical scavengers against MPO-based and NaOCl-based luminol-enhanced CL. Most NSAIDs which affected both MPO and NaOCl-CL appeared to share similar mechanisms, suggesting that MPO oxidant internediates and HOCl are susceptible to NSAID effects. However, most NSAIDs were more effective against MPO-CL. The effect of these NSAIDs against MPO-CL followed the profile of NSAIDs effective in previous studies against PMN-CL. One exception to this was methylprednisone, which has no effect on PMN or MPO-CL, yet inhibited NaOCl-CL. This and other data suggest that MPO and not HOCl-related reactions are a major source of PMN-CL. Less effective NSAIDs affected NaOCl-CL better than MPO-CL. While both HOCl and MPO oxidant intermediates may be affected by NSAIDs, it appears that MPO oxidant intermediates or MPO itself are the primary target for NSAID antioxidant free radical scavenging mechanisms. These antioxidant effects impair the major killing system of the PMN and may be NSAIDs' primary anti-inflammatory mechanism. Although our data suggests the production of superoxide anion and hydroxyl radical from the MPO−H2O2−Cl− reaction, the actual presence or involvement of these free radical species is not confirmed herein.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01965152
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  • 3
    Electronic Resource
    Electronic Resource
    Antioxidation theory of non-steroidal anti-inflammatory drugs based upon the inhibition of luminol-enhanced chemiluminescence from the myeloperoxidase reaction (1982)
    Springer
    Inflammation research 12 (1982), S. 371-376 
    Details
    ISSN: 1420-908X
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The action of non-steroidal anti-inflammatory drugs (NSAIDS) has been ascribed to their ability to block the reaction of arachidonate with cyclooxygenase/peroxidase, thus inhibiting the cellular production of inflammation mediators such as prostaglandins and leukotrienes. However, this and other polymorphonuclear leukocyte (PMN) peroxidases such as myeloperoxidase (MPO) would still be capable of producing destructive oxidants which contribute to inflammation. Sulindac sulfide (Clinoril® sulfide) has recently been shown to scavenge oxidant products of prostaglandin cyclooxygenase/peroxidase and MPO. The MPO−H2O2−Cl− reaction is a potent antimicrobial/cytotoxic system which produces HOCl, a strong oxidant. MPO itself has the ability to oxidize drugs and cellular components, and may be the main oxidant in PMN defenses. An antioxidant/free radical scavenger action of NSAIDs against the MPO system could be a primary mechanism of their anti-inflammatory effects. Other antioxidant/free radical scavengers have anti-inflammatory effects. MPO activity has previously been quantified using chemiluminescence (CL). In this study, NSAIDs from various classes were tested for their ability to inhibit luminol-enhanced CL from MPO. The most potent NSAIDs against MPO-CL were BW755C, phenylbutazone, indomethacin and sulindac sulfide. Salicylates and arylacetic acid derivatives, such as naproxen, also decreased MPO-CL. These drugs are also effective against CL from PMNs, of which MPO may be a main source. This effect of NSAIDs on MPO suggests that NSAIDs may impair the killing mechanism of the PMN, preventing cell destruction and release of inflammation mediators. PMN MPO appears to be a target for the antioxidant/free radical scavenging effects of NSAIDs.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01965406
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  • 4
    Electronic Resource
    Electronic Resource
    Impairment of leukocyte myeloperoxidase bactericidal mechanisms with ketamine (Ketalar®) (1983)
    Springer
    Inflammation research 13 (1983), S. 59-62 
    Details
    ISSN: 1420-908X
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The ability of general anesthetics to depress immune function may lead to increased risk of infection in surgical patients. Recently, halothane, an inhalational anesthetic, was shown to inhibit neutrophil bactericidal mechanisms, the center of which is the reaction of myeloperoxidase with H2O2 and Cl−. This study demonstrates the ability of ketamine, an injectable anesthetic, to interfere with the cytotoxic neutrophil myeloperoxidase-H2O2−Cl− reaction, as tested using a luminol-enhanced chemiluminescence assay. Ketamine, due to its phenolic structure, may scavenge the cytotoxic free radical intermediates of this reaction, as shown previously for non-steroidal anti-inflammatory drugs. This paper, then, identifies a potential mechanism whereby ketamine anesthesia could suppress neutrophil defense mechanisms, thus rendering the surgical patient more susceptible to infection.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01994283
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  • 5
    Electronic Resource
    Electronic Resource
    Attenuation of acute inflammatory effects of silica in rat lung by 21-aminosteroid, U74389G (1995)
    Springer
    Inflammation 19 (1995), S. 9-21 
    Details
    ISSN: 1573-2576
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Chemical alteration of the glucocorticoid, methylprednisolone, has led to the introduction of a new class of compounds called the 21-aminosteroids (21-ASs). The purpose of this study was to investigate the effect of the 21-AS, U74389G, on silica-induced acute lung injury. Male Fischer 344 rats were treated intraperitoneally with saline or U74389G in a total dose of 15 mg/kg divided into three injections of 5 mg/kg separated by 4 h. Following the first treatment, animals from the two groups were intratracheally instilled with silica (10 mg/100 g body wt in 0.5 ml of saline) or saline vehicle (0.5 ml). Twenty-four hours after the instillations, bronchoalveolar lavage (BAL) was performed. In the animals not receiving U74389G, marked increases in total protein, (β-glucuronidase, and lactate dehydrogenase (LDH) activities and number of neutrophils (PMNs) were demonstrated in the BAL fluid of the silica-treated animals compared to their controls. Silica also caused dramatic increases in the luminol-dependent chemiluminescence (CL) of lung tissue and BAL cells. The CL reaction was decreased by superoxide dismutase (SOD) andN-nitro-l-arginine methyl ester hydrochloride (L-NAME), a nitric oxide (NO) synthase inhibitor. In animals treated with U74389G, there was attenuation of the silica-induced increases in biochemical, cellular, and chemiluminescent indices of damage. This study demonstrates that U74389G significantly reduces acute lung injury caused by the intratracheal instillation of silica, and this drug may be of potential value for treatment of lung diseases in which damage caused by reactive oxygen species has been implicated.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01534376
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  • 6
    Electronic Resource
    Electronic Resource
    Granulocyte response to oxidized FMLP (1984)
    Springer
    Inflammation 8 (1984), S. 87-99 
    Details
    ISSN: 1573-2576
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract We prepared FMoxLP by oxidation of FMLP and evaluated its ability to trigger a variety of granulocyte responses. FMoxLP was found to depolarize granulocyte membranes; increase granulocyte oxygen consumption, superoxide production, and hydrogen peroxide production; compete with FMLP for binding to granulocytes; and stimulate granulocyte chemotaxis. Against all of these granulocyte functions, FMoxLP was considerably less potent than the parent FMLP. When luminol-dependent-granulocyte chemiluminescence (CL) was studied, FMoxLP was observed to be a more potent stimulus of this response than FMLP. This increased CL activity of FMoxLP may be related to nonoxidative burst mechanisms. Our results indicate that FMoxLP retains a significant amount of the biological activity of FMLP (albeit in general less potent). The biological importance of the observed activities of FMoxLP must await further investigation.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00918356
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  • 7
    Electronic Resource
    Electronic Resource
    Inhibition by nonsteroidal antiinflammatory drugs of luminol-dependent human-granulocyte chemiluminescence and [3H]FMLP binding (1982)
    Springer
    Inflammation 6 (1982), S. 113-125 
    Details
    ISSN: 1573-2576
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract A system is described to evaluate for nonsteroidal antiinflammatory drugs by means of luminol-dependent human-granulocyte chemiluminescence (CL) is described. The CL is produced using either opsonized zymosan (yeast cells) or the soluble chemotactic peptide f-Met-Leu-Phe as the perturbant of the granulocyte membrane. Using either system, the following drug effects 2×10−5 M were noted: only sulindac sulfide, and not sulindac sulfone or sulindac, displayed marked inhibition of chemiluminescence, following the in vivo data regarding inflammatory effects. The 5-OH indomethacin metabolite was likewise inactive as an inhibitor of CL mirroring in vivo effects. MK(+)410, MK(−)830 and MK835 all showed approximately 50% inhibition of CL, displaying deviation from in vivo data. MK(+)830 markedly stimulated CL, 4–6 times the control (without drug), which is clearly different from its enantiomer, MK(−)830. The reasons for this behavior are unclear. However, receptor binding studies with [3H]FMLP were accomplished in the presence and absence of the various drugs at 2×105 M that were effective inhibitors of chemiluminescence (CL). Indomethacin, MK(−)830 and MK(+)410 had equivalent percent control binding and percent control CL. Sulindac sulfide and MK(+)835 both had higher percent control binding than percent control CL, with MK(+)835 displaying apparent increased numbers of available receptors relative to control. MK(+)830, which produces large increases in CL, produced a minor effect on percent control binding. A direct relationship between binding and CL does not exist with each drug. Chemiluminescence is dependent on ion movement and oxidative metabolism and is a secondary event to agonist-receptor occupation.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00910724
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  • 8
    Electronic Resource
    Electronic Resource
    A new screening method to detect water-soluble antioxidants: acetaminophen (tylenol®) and other phenols react as antioxidants and destroy peroxynitrite-based luminol-dependent chemiluminescence (1998)
    New York : Wiley-Blackwell
    Journal of Bioluminescence and Chemiluminescence 13 (1998), S. 339-348 
    Details
    ISSN: 0884-3996
    Keywords: peroxynitrite ; antioxidants ; luminol ; acetaminophen ; phenols ; catecholamines ; norepinephrine ; isoproterenol ; epinephrine ; SIN-1 ; sydnonimines ; polyphenols ; catechins ; Chemistry ; Biochemistry and Biotechnology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology
    Notes: This study is based on a simple chemical interaction of peroxynitrite (O=N—O—O-) and luminol, which produces blue light upon oxidation. Since peroxynitrite has a half-life of about 1 s, a drug known as linsidomine (SIN-1) is used as a peroxynitrite generator. Peroxynitrite can oxidize lipids, proteins and nucleic acids. Upon the stimulation of inflammation and/or infection, macrophages and neutrophils can be induced to produce large amounts of peroxynitrite, which can oxidize phenols and sulphhydryl-containing compounds. Therefore, phenols and sulphhydryls eliminate peroxynitrite. This is an example of the Yin-Yang hypothesis e.g. oxidation-reduction. Acetaminophen (Tylenol®) can inhibit fever and some types of pain without being a particularly effective anti-inflammatory. Since it is a phenol, it could act as a nitration target for peroxynitrite. Then peroxynitrite, the possible cause of pain and elevated temperature, might be destroyed in the reaction. Acetaminophen is a phenolic compound which produces a clear inhibitory dose-response curve with peroxynitrite in its range of clinical effectiveness. Whether acetaminophen actually works as we suggest is to be proven. Three different types of reaction could decrease the amount of peroxynitrite: (a) interference with base-catalysed opening of the SIN-1 molecule; (b) destruction of one or both substances needed to form it -  superoxide and/or nitric oxide; when the SIN-1 degrades to superoxide and nitric oxide, the former may be destroyed by superoxide dismutase (SOD); (c) peroxynitrite may react directly with phenols (mono-, di-, tri- and tetraphenols), possibly by nitration. Nordihydroguaiaretic acid and 2-hydroxyestradiol (catechol estrogen) are potent inhibitors of luminol light emission. Epineprine, isoproterenol, pyrogallol, catechol and ascorbic acid (a classic antioxidant) are all inhibitors of luminol chemiluminescence. Isoproterenol, norepinephrine/and epinephrine first inhibit light but overall stimulate the light production. Initially, SIN-1 degrades to produce peroxynitrite, which reacts with luminol to produce blue light. If any of three catecholamines are present with the reaction that produces light, there is an initial inhibition of light production, and then a marked stimulation. A possible reason for this is that these catechols are oxidized and the metabolized phenol stimulates the production of light from luminol. Also, during oxidation of catecholamines superoxide is sometimes formed, which could stimulate production of peroxynitrite. This simple screening system is introduced to find useful antioxidants against peroxynitrite. © 1998 John Wiley & Sons, Ltd.
    Additional Material: 8 Ill.
    Type of Medium: Electronic Resource
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