Publications
173 results found
Williams EA, Quinlan GJ, Goldstraw P, et al., 1998, Postoperative lung injury and oxidative damage in patients undergoing pulmonary resection, EUROPEAN RESPIRATORY JOURNAL, Vol: 11, Pages: 1028-1034, ISSN: 0903-1936
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- Citations: 54
Salmon M, Koto H, Lynch OT, et al., 1998, Proliferation of airway epithelium after ozone exposure - Effect of apocynin and dexamethasone, AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE, Vol: 157, Pages: 970-977, ISSN: 1073-449X
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- Citations: 47
Niebauer J, Webb-Peploe KM, Jourdan K, et al., 1998, Chronic exercise training modulates oxidative stress in patients with chronic heart failure, JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY, Vol: 31, Pages: 509A-509A, ISSN: 0735-1097
Brett SJ, Quinlan GJ, Mitchell J, et al., 1998, Production of nitric oxide during surgery involving cardiopulmonary bypass, CRITICAL CARE MEDICINE, Vol: 26, Pages: 272-278, ISSN: 0090-3493
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- Citations: 52
Salmon M, Koto H, Lynch OT, et al., 1998, Proliferation of airway epithelium after ozone exposure: Effect of apocynin and dexamethasone, American Journal of Respiratory and Critical Care Medicine, Vol: 157, Pages: 970-977, ISSN: 1073-449X
Ozone is an environmental pollutant with potent oxidizing properties. We investigated whether exposure to ozone-induced cell proliferation in the lungs of rats, and determined the effect of an antioxidant and of a glucocorticosteroid in Brown-Norway (BN) rats. Following single ozone exposure (0.5, 1.0, or 3.0 ppm for 6 h), proliferating cell nuclear antigen (PCNA) expression, as determined with immunohistochemistry, was significantly increased in the bronchial epithelium and alveolar epithelium as compared with controls exposed to filtered air with a maximal effect at 24 to 48 h (p < 0.001). Apocynin (5 mg/kg, orally), a reduced nicotinamide adenine dinucleotide phosphate (NADPH) oxidase inhibitor, reduced the PCNA index in bronchial epithelium induced by ozone (3 ppm, 6 h) from 11.5 ± 1.3% (percent of nuclear cells expressing PCNA) to 4.4 ± 1.3% (mean ± SEM; p < 0.05). Dexamethasone (3 mg/kg, intraperitoneally) also reduced the PCNA index in bronchial epithelium, from 19.2 ± 2.3% to 10.9 ± 2.6% (p < 0.05). Dexamethasone but not apocynin inhibited ozone-induced neutrophil influx. Rats exposed repeatedly to ozone (3.0 ppm, 3 h, on three occasions 48 h apart) expressed a lower PCNA index in bronchial epithelium than did rats exposed only once at 1.9 ± 0.7% versus 6.0 ± 0.9%, respectively (p < 0.05). The proliferative epithelial response following a single exposure to ozone is modulated through oxidative and inflammatory mechanisms probably in-volving neutrophils.
Gutteridge JMC, Quinlan GJ, Kovacic P, 1998, Phagomimetic action of antimicrobial agents, FREE RADICAL RESEARCH, Vol: 28, Pages: 1-14, ISSN: 1071-5762
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- Citations: 29
Quinlan GJ, Lamb NJ, Evans TW, et al., 1998, Increased levels of markers of protein oxidation in bronchoalveolar lavage fluid from patients with ARDS, NATO Advanced Study Institute on Acute Respiratory Distress Syndrome - Cellular and Molecular Mechanisms and Clinical Management, Publisher: PLENUM PRESS DIV PLENUM PUBLISHING CORP, Pages: 263-264, ISSN: 0258-1213
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- Citations: 1
Gutteridge JMC, Quinlan GJ, Yamamoto Y, 1998, Hypothesis - Are fatty acid patterns characteristic of essential fatty acid deficiency indicative of oxidative stress?, FREE RADICAL RESEARCH, Vol: 28, Pages: 109-114, ISSN: 1071-5762
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- Citations: 24
Chen Y, Quinlan GJ, Evans TW, et al., 1997, Tissue distribution of constitutive and inducible haem oxygenase mRNA in normal and lipopolysaccharide (LPS) treated rats, Thorax, Vol: 52, ISSN: 0040-6376
Haem oxygenase catalyses the conversion of haem to biliverdin, free iron, and CO. It exists in two isoforms, one is constitutively expressed (HO-2), the other (HO-1) is induced by a variety of stresses including haem, endotoxin and hyperthermia. HO-1 is a heat shock protein (HSP) and is known as HSP 32. Evidence, suggests that haem oxygenase, has antioxidant properties and that its induction protects against oxidative damage. Production of bilirubin, a known antioxidant, from biliverdin may partly be responsible for these effects. Sepsis is often a complication of ARDS, and induction of heat shock proteins may help protect against tissue damage associated with the onset of ARDS. We have used a rat model of endotoxemia to establish the distribution of HO-1 and HO-2 mRNA expression in different tissues and compared these to normal healthy rats. (See table). *P<0.05. n=4. Units are HO mRNA / β-actin mRNA. Kidney Diaphrame Liver Spleen Lung HO-1 Normal 0,180 ± 0,072* 2,198 ± 0,844 3,145 ± 0,903 1,640 ± 0,216 0,395 ± 0,124* HO-1 LPS 2,615 ± 0,746* 5,300 ± 1,493 4,057 ± 0,921 1,803 ± 0,956 1,410 ± 0,135* HO-2 Normal 2,970 ± 0,952 8,812 ± 1,994 4,460 ± 1,063 1,047 ± 0,232 0,978 ± 0,418 HO-2 LPS 2,488 ± 0,432 6,928 ± 2,035 2,430 ± 0,920 0,802 ± 0,311 0,855 ± 0,385 In normal healthy rats HO-2 mRNA predominates in all tissues except the spleen. However, after 4 hours treatment with endotoxin significant upregulation of HO-1 is seen in most tissues. In particular, the lung and trachea show pronounced HO-1 mRNA upregulation, which in the case of the trachea is a novel finding. Induction of this protein may represent one of the first lines of defence against lung associated oxidative stress and have implications for ARDS and sepsis in patients.
Lamb NJ, Hamilton L, Quinlan GJ, et al., 1997, Is heme oxygenase present in plasma and BALF from patients with ARDS?, Thorax, Vol: 52, ISSN: 0040-6376
Heme oxygenase is the microsomal-bound enzyme responsible for cleavage of heme to biliverdin, with the concomitant release of free iron and carbon monoxide. Two isoforms have been identified and cloned: HO-1 (inducible) and HO-2 (constitutive). HO-1 (heat shock protein 32) is induced by various forms of oxidative stress, where it is thought to have a "protective" effect through the production of bilirubin and induction of ferritin. Patients with ARDS are known to be under severe oxidative stress and the expression of heat shock proteins in these patients has been well established. Here, we analysed plasma and bronchoalveolar lavage fluid (BALF) samples from patients with ARDS to see if HO-1 was released into extracellular fluids. BALF samples from 7 patients with ARDS and 3 intensive care controls were routinely collected, spun to remove cellular debris and mucus, and stored at -80°C until use. Blood samples from 6 patients with ARDS and 4 healthy controls were collected, the plasma obtained by centrifugation, and stored at -80°C. The presence of heme oxygenase was determined using standard immunoblotting (Western) techniques and levels indexed to a 2ng sample of the recombinant enzyme. Using this technique, we found no evidence for the presence of HO-1 in plasma or BALF in either patients with ARDS or control groups. If heme oxygenase is present in extracellular fluids then it is below 2ng, or rapidly degraded by proteolytic enzymes to impair immunoreactivity. These possibilities are currently under investigation.
Jourdan KB, Evans TW, Quinlan G, et al., 1997, Oxidant stress induces the release of both PGE<inf>2</inf> and 8-iso PGF<inf>2α</inf> by a COX-2 dependent pathway, Thorax, Vol: 52, ISSN: 0040-6376
Introduction 8-iso prostaglandin (PG) F2α is one of a series of prostaglandin-like compounds the isoprostanes. 8-iso PGF2α has been shown to have potent vasoactive properties on both rat and human pulmonary artery (PA). Their synthesis was initially described as independent of the enzyme cyclooxygenase and through free radical action on arachidonic acid, although recent evidence suggests the involvement of cyclooxygenase. We have compared the release of PGE2 (a typical COX metabolite) and 8-iso PGF2α from human PA smooth muscles cells subjected to oxidant stress by a combination of xanthine oxidase (XO) and its substrate hypoxanthine (HX). Methods Human PA smooth muscle cells were cultured by explant from human PA denuded of endothelium in culture medium containing 20% foetal calf serum. PGE2 was measured by radioimmumoassay and 8-iso PGF2α by enzyme immunoassay. Cell respiration was measured by the conversion of 3-[4,5-dimethylthiazol-2-yl]-2,5-diphenyl tetrazolium bromide to a blue formazan product. Results 8-iso PGF2α was increased approximately two-fold after incubation with XO and it's substrate HX compared to XO alone. This ratio of increase was the same for PGE2 (fig. A). Oxidant stress was confirmed by a reduction of cellular respiration in the presence of XO and HX (fig. B). The release of both the prostanoids was inhibited more than 80% by the COX-2 specific inhibitor L-745,337. Similar observations were made when prostanoid release was stimulated by cytokines. (Graph Presented) Conclusion Oxidant stress stimulates the release of the isoporstane, 8-iso PGF2α and the typical COX metabolite, PGE2. Moreover, COX-2 appears to be important in the release of both prostanoids. These observations may help to explain why prostaglandin and isoprostane release is increased in conditions of oxidant stress.
Mumby S, Margarson M, Quinlan GJ, et al., 1997, Is bleomycin-detectable iron present in the plasma of patients with septic shock?, INTENSIVE CARE MEDICINE, Vol: 23, Pages: 635-639, ISSN: 0342-4642
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- Citations: 14
Chabot F, Mitchell JA, Quinlan GJ, et al., 1997, Characterization of the vasodilator properties of peroxynitrite on rat pulmonary artery: Role of poly(adenosine 5'-diphosphoribose) synthase, BRITISH JOURNAL OF PHARMACOLOGY, Vol: 121, Pages: 485-490, ISSN: 0007-1188
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- Citations: 51
Messent M, Sinclair DG, Quinlan GJ, et al., 1997, Pulmonary vascular permeability after cardiopulmonary bypass and its relationship to oxidative stress, CRITICAL CARE MEDICINE, Vol: 25, Pages: 425-429, ISSN: 0090-3493
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- Citations: 51
Quinlan GJ, Lamb NJ, Tilley R, et al., 1997, Plasma hypoxanthine levels in ARDS: Implications for oxidative stress, morbidity, and mortality, AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE, Vol: 155, Pages: 479-484, ISSN: 1073-449X
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- Citations: 144
Chabot F, Mitchell JA, Quinlan G, et al., 1996, Role of poly-ADP ribosyltransferase in the vasodilator actions of peroxynitrite, Thorax, Vol: 51, ISSN: 0040-6376
The pulmonary vasculature is constantly exposed to oxygen species such as nitric oxide (NO) and superoxide anions which are usually metabolised by anti-oxidant enzymes. However, during inflammatory conditions, oxidants may be formed in excess leading to cellular damage or dysfunction. NO reacts rapidly with superoxide anions to form the putative toxic oxidant, peroxynitrite ONOO-. ONOO- has been shown to activate poly-ADP ribosyltransferase (PARS) leading to a depletion NAD+ and ATP, an event that is likely to greatly compromise energetic processes such as the maintenance of vascular tone. We have shown that ONOO- is a vasodilator of rat pulmonary arteries. Thus, we have investigated the possible contribution of PARS activation in the vasodilator properties of ONOO-. Pulmonary arteries were cut into rings and mounted in 2 ml organ baths containing warmed (37°C) and gassed (95%O2:5%CO2) Krebs' buffer. Tone (0.5 g) was induced by the addition of U46619 (1×10-6M). Under these conditions ONOO- (1×10-6-1×10-4M), acetylcholine (1×10-8-1×10-6M), and sodium nitroprusside (1×10-8-1×10-6M) caused concentration-dependent relaxation of pulmonary arteries. The NO synthase inhibitor, NG-nitro-L-arginine methyl ester (1×10-4M), inhibited the effects of acetylcholine but not ONOO- or sodium nitroprusside. Superoxide dismutase had no effect on any of the vasodilator agents. The PARS inhibitor 3-aminobenzamide (1×10-2M) significantly inhibited the relaxation caused by ONOO- but did not effect that caused by acetylcholine or sodium nitroprusside. Thus, ONOO- relaxes rat pulmonary artery directly, without causing the release of NO or superoxide. Moreover, ONOO-, unlike endogenously released NO (by acetylcholine) or nitrovasodilators appears to cause relaxation by activation of PARS. We propose that ONOO- activates PARS resulting in the depletion of cellular ATP reducing active processes of vascular smooth muscle including vaso-c
Quinlan GJ, Lamb NJ, Evans TW, et al., 1996, Pro-oxidant hypoxanthine and xanthine in the plasma of patients with ARDS, Thorax, Vol: 51, ISSN: 0040-6376
Xanthine oxidase (XOD) has been implicated as a source of reactive oxygen species (ROS) in vivo, and may contribute to oxidative damage associated with some disease states including ARDS.It is formed from the dehydrogenase form of the enzyme (XDH) by a variety of causes including ischaemia/reperfusion and hypoxia. XOD utilises its substrates hypoxanthine and xanthine to produce uric acid, superoxide and hydrogen peroxide. These ROS whilst not particularly damaging themselves, are capable of forming more aggressive species such as peroxynitrite and the hydroxyl radical. It has been reported that hypoxanthine levels are increased in the plasma of ARDS patients compared to normal controls, and also in critically ill patients, possibly because of impaired ATP metabolism due to hypoxia. We have measured plasma hypoxanthine and xanthine levels by hplc in 14 surviving (N =118) and 14 non-surviving (N = 114) patients with ARDS. Xanthine levels were not found to be significantly different between the two groups, although levels were significantly increased compared to normal healthy controls. However, hypoxanmine levels were found to be highly significantly increased (p < 0.0001) in ARDS non-survivors (36.06 ± 3.094 μmols) compared to survivors (17.99 ± 2.26 μmols). Additionally when hypoxanthine levels were compared with plasma protein thiol levels (a possible marker of oxidative damage in ARDS patients) a significant negative correlation was found (p < 0.05). These results suggest an involvement of XOD in the morbidity of ARDS, and may indicate that hypoxia is an important contributing factor to the severe oxidative stress.
Chabot F, Mitchell JA, Quinlan G, et al., 1996, Peroxynitrite is a vasodilator of rat pulmonary arteries at concetrations that do not cause endothelial dysfunction, Thorax, Vol: 51, ISSN: 0040-6376
Under physiological conditions, the potent dilator gas, nitric oxide (NO) is continuously released by endothelial cells to maintain organ blood flow. Endothelial derived NO is catalysed by endothelial NO synthase (eNOS), which my virtue of its calcium dependency, forms discreet quanta of NO. Under inflammatory conditions, such as occur in septic shock, a calcium-independent isoform of NOS is expressed (iNOS) that produces copious amounts of NO, a process which is thought to contribute to the fall in blood pressure seen in clinical sepsis. In sepsis the presence of large amounts of activated leukocytes results in elevated levels of superoxide anions (O2-) which are known to react rapidly with NO to form the potent oxidant peroxynitrite (ONOO-). Recent reports have described ONOO- as a toxic oxidant that could contribute to endothelium dysfunction in diseases such as septic shock. Since the pulmonary vasculature represents a prime site for oxidant formation, we have characterised the effects of authentic ONOO- on vascular tone in isolated rat pulmonary arteries. Pulmonary arteries were cut into rings and mounted in 2 ml organ baths containing warmed (37°C) and gassed (95%O2:5%oCO2) Krebs' buffer. ONOO- (1×10-6-1×10-4M) had no effect on resting tone but caused concentration-dependent vasodilatation in vessels pre-contracted (1 g) with the thomboxane mimetic, U46619 (1×10-6M). Similarly both acetylcholine (endothelium-dependant) and sodium nitroprusside (endothelium-independent) caused relaxation of pre-contracted pulmonary arteries. In separate experiments we found that pre-incubation of pulmonary arteries with ONOO-, had no effect on subsequent responses to acetylcholine or sodium nitroprusside. Thus, ONOO- is a vasodilator of rat pulmonary arteries at concentrations that do not cause vascular dysfunction. These observations detract from ONOO- being a toxic species in the pulmonary vasculature. ONOO- causes relaxation in the μM range whereas N
Gutteridge JMC, Mumby S, Quinlan GJ, et al., 1996, Pro-oxidant iron is present in human pulmonary epithelial lining fluid: Implications for oxidative stress in the lung, BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, Vol: 220, Pages: 1024-1027, ISSN: 0006-291X
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- Citations: 92
Quinlan GJ, Lamb NJ, Evans TW, et al., 1996, Plasma fatty acid changes and increased lipid peroxidation in patients with adult respiratory distress syndrome, CRITICAL CARE MEDICINE, Vol: 24, Pages: 241-246, ISSN: 0090-3493
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- Citations: 93
Messent M, Griffiths MJD, Quinlan GJ, et al., 1996, Ischaemia-reperfusion injury in the rat is modulated by superoxide generation and leads to an augmentation of the hypoxic pulmonary vascular response, CLINICAL SCIENCE, Vol: 90, Pages: 47-54, ISSN: 0143-5221
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- Citations: 10
SINCLAIR DG, HASLAM PL, QUINLAN GJ, et al., 1995, THE EFFECT OF CARDIOPULMONARY BYPASS ON INTESTINAL AND PULMONARY ENDOTHELIAL PERMEABILITY, CHEST, Vol: 108, Pages: 718-724, ISSN: 0012-3692
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- Citations: 103
QUINLAN GJ, MUMBY S, PEPPER J, et al., 1994, PLASMA 4-HYDROXY-2-NONENAL LEVELS DURING CARDIOPULMONARY BYPASS, AND THEIR RELATIONSHIP TO THE IRON-LOADING OF TRANSFERRIN, BIOCHEMISTRY AND MOLECULAR BIOLOGY INTERNATIONAL, Vol: 34, Pages: 1277-1282, ISSN: 1039-9712
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- Citations: 12
BINGHAM BR, QUINLAN GJ, TARELLI E, 1994, IRON-BINDING AFFINITY OF BACTERIAL VACCINE POLYSACCHARIDES WHICH CONTAIN PHOSPHODIESTER LINKAGES AS PART OF THE POLYMER-CHAIN AND OF OTHER POLYPHOSPHATES, INCLUDING DNA, JOURNAL OF PHARMACY AND PHARMACOLOGY, Vol: 46, Pages: 1000-1003, ISSN: 0022-3573
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- Citations: 2
GUTTERIDGE JMC, QUINLAN GJ, MUMBY S, et al., 1994, PRIMARY PLASMA ANTIOXIDANTS IN ADULT-RESPIRATORY-DISTRESS-SYNDROME PATIENTS - CHANGES IN IRON-OXIDIZING, IRON-BINDING, AND FREE RADICAL-SCAVENGING PROTEINS, JOURNAL OF LABORATORY AND CLINICAL MEDICINE, Vol: 124, Pages: 263-273, ISSN: 0022-2143
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- Citations: 46
GUTTERIDGE JMC, QUINLAN GJ, EVANS TW, 1994, TRANSIENT IRON OVERLOAD WITH BLEOMYCIN DETECTABLE IRON IN THE PLASMA OF PATIENTS WITH ADULT-RESPIRATORY-DISTRESS-SYNDROME, THORAX, Vol: 49, Pages: 707-710, ISSN: 0040-6376
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- Citations: 35
GUTTERIDGE JMC, QUINLAN GJ, SWAIN J, et al., 1994, FERROUS ION FORMATION BY FERRIOXAMINE PREPARED FROM AGED DESFERRIOXAMINE - A POTENTIAL PROOXIDANT PROPERTY, FREE RADICAL BIOLOGY AND MEDICINE, Vol: 16, Pages: 733-739, ISSN: 0891-5849
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- Citations: 16
QUINLAN GJ, EVANS TW, GUTTERIDGE JMC, 1994, LINOLEIC-ACID AND PROTEIN THIOL CHANGES SUGGESTIVE OF OXIDATIVE DAMAGE IN THE PLASMA OF PATIENTS WITH ADULT-RESPIRATORY-DISTRESS-SYNDROME, FREE RADICAL RESEARCH, Vol: 20, Pages: 299-306, ISSN: 1071-5762
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- Citations: 20
QUINLAN GJ, EVANS TW, GUTTERIDGE JMC, 1994, OXIDATIVE DAMAGE TO PLASMA-PROTEINS IN ADULT-RESPIRATORY-DISTRESS-SYNDROME, FREE RADICAL RESEARCH, Vol: 20, Pages: 289-298, ISSN: 1071-5762
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- Citations: 82
QUINLAN GJ, EVANS TW, GUTTERIDGE JMC, 1994, 4-HYDROXY-2-NONENAL LEVELS INCREASE IN THE PLASMA OF PATIENTS WITH ADULT-RESPIRATORY-DISTRESS-SYNDROME AS LINOLEIC-ACID APPEARS TO FALL, FREE RADICAL RESEARCH, Vol: 21, Pages: 95-106, ISSN: 1071-5762
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- Citations: 29
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