Imperial College London

DrGregoryQuinlan

Faculty of MedicineNational Heart & Lung Institute

Senior Research Fellow
 
 
 
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g.quinlan

 
 
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Location

 

B140BGuy Scadding BuildingRoyal Brompton Campus

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Summary

 

Publications

Publication Type
Year
to

157 results found

Quinlan GJ, Lamb NJ, Evans TW, Gutteridge JMCet 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.

Journal article

Chabot F, Mitchell JA, Quinlan G, Evans TWet 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

Journal article

Gutteridge JMC, Mumby S, Quinlan GJ, Chung KFet 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

Journal article

Quinlan GJ, Lamb NJ, Evans TW, Gutteridge JMCet 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

Journal article

Messent M, Griffiths MJD, Quinlan GJ, Gutteridge JMC, Evans TWet 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

Journal article

SINCLAIR DG, HASLAM PL, QUINLAN GJ, PEPPER JR, EVANS TWet al., 1995, THE EFFECT OF CARDIOPULMONARY BYPASS ON INTESTINAL AND PULMONARY ENDOTHELIAL PERMEABILITY, CHEST, Vol: 108, Pages: 718-724, ISSN: 0012-3692

Journal article

QUINLAN GJ, MUMBY S, PEPPER J, GUTTERIDGE JMCet 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

Journal article

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

Journal article

GUTTERIDGE JMC, QUINLAN GJ, MUMBY S, HEATH A, EVANS TWet 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

Journal article

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

Journal article

GUTTERIDGE JMC, QUINLAN GJ, SWAIN J, COX Jet 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

Journal article

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

Journal article

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

Journal article

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

Journal article

MOAT NE, EVANS TE, QUINLAN GJ, GUTTERIDGE JMCet al., 1993, CHELATABLE IRON AND COPPER CAN BE RELEASED FROM EXTRACORPOREALLY CIRCULATED BLOOD DURING CARDIOPULMONARY BYPASS, FEBS LETTERS, Vol: 328, Pages: 103-106, ISSN: 1873-3468

Journal article

MESSENT M, QUINLAN GJ, GRIFFITHS MJD, GUTTERIDGE JMC, EVANS TWet al., 1993, CHARACTERIZATION OF ISCHEMIA/REPERFUSION DAMAGE IN AN ISOLATED-PERFUSED RAT LUNG, AMERICAN REVIEW OF RESPIRATORY DISEASE, Vol: 147, Pages: A931-A931, ISSN: 0003-0805

Journal article

GUTTERIDGE JMC, QUINLAN GJ, 1993, ANTIOXIDANT PROTECTION AGAINST ORGANIC AND INORGANIC OXYGEN RADICALS BY NORMAL HUMAN PLASMA - THE IMPORTANT PRIMARY ROLE FOR IRON-BINDING AND IRON-OXIDIZING PROTEINS, BIOCHIMICA ET BIOPHYSICA ACTA, Vol: 1156, Pages: 144-150, ISSN: 0006-3002

Journal article

GUTTERIDGE JMC, QUINLAN GJ, 1992, ANTIOXIDANT PROTECTION AGAINST ORGANIC AND INORGANIC OXYGEN RADICALS BY NORMAL HUMAN PLASMA - THE IMPORTANT PRIMARY ROLE FOR IRON-BINDING AND IRON-OXIDIZING PROTEINS, BIOCHIMICA ET BIOPHYSICA ACTA, Vol: 1159, Pages: 248-254, ISSN: 0006-3002

Journal article

QUINLAN GJ, COUDRAY C, HUBBARD A, GUTTERIDGE JMCet al., 1992, VANADIUM AND COPPER IN CLINICAL SOLUTIONS OF ALBUMIN AND THEIR POTENTIAL TO DAMAGE PROTEIN-STRUCTURE, JOURNAL OF PHARMACEUTICAL SCIENCES, Vol: 81, Pages: 611-614, ISSN: 0022-3549

Journal article

REDHEAD K, QUINLAN GJ, DAS RG, GUTTERIDGE JMCet al., 1992, ALUMINUM-ADJUVANTED VACCINES TRANSIENTLY INCREASE ALUMINUM LEVELS IN MURINE BRAIN-TISSUE, PHARMACOLOGY & TOXICOLOGY, Vol: 70, Pages: 278-280, ISSN: 0901-9928

Journal article

QUINLAN GJ, GUTTERIDGE JMC, 1991, DNA-BASE DAMAGE BY BETA-LACTAM, TETRACYCLINE, BACITRACIN AND RIFAMYCIN ANTIBACTERIAL ANTIBIOTICS, BIOCHEMICAL PHARMACOLOGY, Vol: 42, Pages: 1595-1599, ISSN: 0006-2952

Journal article

ARUOMA OI, HALLIWELL B, LAUGHTON MJ, QUINLAN GJ, GUTTERIDGE JMCet al., 1989, THE MECHANISM OF INITIATION OF LIPID-PEROXIDATION - EVIDENCE AGAINST A REQUIREMENT FOR AN IRON(II) IRON(III) COMPLEX, BIOCHEMICAL JOURNAL, Vol: 258, Pages: 617-620, ISSN: 0264-6021

Journal article

QUINLAN GJ, GUTTERIDGE JMC, 1989, BACITRACIN AND A BACITRACIN-ZINC COMPLEX DAMAGE DNA AND CARBOHYDRATE IN THE PRESENCE OF IRON AND COPPER-SALTS, FREE RADICAL RESEARCH COMMUNICATIONS, Vol: 7, Pages: 37-44, ISSN: 8755-0199

Journal article

QUINLAN GJ, HALLIWELL B, MOORHOUSE CP, GUTTERIDGE JMCet al., 1988, ACTION OF LEAD(II) AND ALUMINUM(III) IONS ON IRON-STIMULATED LIPID-PEROXIDATION IN LIPOSOMES, ERYTHROCYTES AND RAT-LIVER MICROSOMAL FRACTIONS, BIOCHIMICA ET BIOPHYSICA ACTA, Vol: 962, Pages: 196-200, ISSN: 0006-3002

Journal article

QUINLAN GJ, GUTTERIDGE JMC, 1988, HYDROXYL RADICAL GENERATION BY THE TETRACYCLINE ANTIBIOTICS WITH FREE-RADICAL DAMAGE TO DNA, LIPIDS AND CARBOHYDRATE IN THE PRESENCE OF IRON AND COPPER-SALTS, FREE RADICAL BIOLOGY AND MEDICINE, Vol: 5, Pages: 341-348, ISSN: 0891-5849

Journal article

QUINLAN GJ, GUTTERIDGE JMC, 1988, OXIDATIVE DAMAGE TO DNA AND DEOXYRIBOSE BY BETA-LACTAM ANTIBIOTICS IN THE PRESENCE OF IRON AND COPPER-SALTS, FREE RADICAL RESEARCH COMMUNICATIONS, Vol: 5, Pages: 149-158, ISSN: 8755-0199

Journal article

QUINLAN GJ, GUTTERIDGE JMC, 1987, OXYGEN RADICAL DAMAGE TO DNA BY RIFAMYCIN-SV AND COPPER IONS, BIOCHEMICAL PHARMACOLOGY, Vol: 36, Pages: 3629-3633, ISSN: 0006-2952

Journal article

Moorhouse PC, Grootveld M, Halliwell B, Quinlan JG, Gutteridge JMet al., 1987, Allopurinol and oxypurinol are hydroxyl radical scavengers., FEBS Lett, Vol: 213, Pages: 23-28, ISSN: 0014-5793

Allopurinol is a scavenger of the highly reactive hydroxyl radical (k2 approx. 10(9) M-1 X s-1). One product of attack of hydroxyl radical upon allopurinol is oxypurinol, which is a major metabolite of allopurinol. Oxypurinol is a better hydroxyl radical scavenger than is allopurinol (k2 approx. 4 X 10(9) M-1 X s-1) and it also reacts with the myeloperoxidase-derived oxidant hypochlorous acid. Hence the protective actions of allopurinol against reperfusion damage after hypoxia need not be entirely due to xanthine oxidase inhibition.

Journal article

GUTTERIDGE JMC, QUINLAN GJ, 1986, CARMINIC ACID-PROMOTED OXYGEN RADICAL DAMAGE TO LIPID AND CARBOHYDRATE, FOOD ADDITIVES AND CONTAMINANTS PART A-CHEMISTRY ANALYSIS CONTROL EXPOSURE & RISK ASSESSMENT, Vol: 3, Pages: 289-293, ISSN: 1944-0049

Journal article

GUTTERIDGE JMC, BEARD APC, QUINLAN GJ, 1985, CATALASE ENHANCES DAMAGE TO DNA BY BLEOMYCIN-IRON(II) - THE ROLE OF HYDROXYL RADICALS, BIOCHEMISTRY INTERNATIONAL, Vol: 10, Pages: 441-449, ISSN: 0158-5231

Journal article

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