Gutteridge

Gutteridge, J.M. Halliwell, B. (1988). The deoxyribose assay an assay both for free hydroxyl radical and for site-specific hydroxyl radical production. Biochemical Journal, Vol. 253, (April 1988), pp. 932-933, ISSN 0264-6021. 

Halliwell, B. and Gutteridge, J.M.C. (1986). Oxygen free radicals and iron in relation to biology and medicine—some problems and concepts. Archives of Biochemistry and Biophysics 246, 501-514. 

Bernard SA, Gray TW, Buist MD, Jones BM, Silvester W, Gutteridge G, Smith K. Treatment of comatose survivors of out-of-hospital cardiac arrest with induced h)fpother-mia. N Engl J Med 2002 346 557-563. 

HOLZHERR M L, RETALLACK R W, GUTTERIDGE D H, PRICE R I, FAULKNER D L, WILSON S G, WILL R K, STEWART G O, STUCKEY B G, PRINCE R L, CRIDDLE R A, KENT G N, BHAGAT C I, DHALIWAL S s and JAMROZIK k (2000) Calcium absorption in postmenopausal osteoporosis Benefit of HRT plus calcitriol, but not HRT alone, in both malabsorbers and normal absorbers. Osteoporosis Int 11, 43-51. 

Gutteridge, J.M.C. (1987). Bleomycin-detectable iron in knee-joint synovial fluid from arthritic patients and its relationship to the extracellular activities of caeruloplasmin, transferrin and lactoferrin. Biochem. J. 245, 415-421. 

Gutteridge, J.M.C. (1988) In Oxygen Radicals and Tissue Injury (ed. B. Halliwell) pp. 9-19, Upjohn and Federal American Societies for Experimental Biology, Bethesda, MD. 

Halliwell, B., Grootveld, M. and Gutteridge, J.M.C. (1988). Methods for the specific detection of hydroxyl radical in Methods in Biochemical Analysis (ed. D. Click) pp. 59-90, John Wiley and Sons. 

Rowley, A., Gutteridge, J.M.C., Blake, D.R, Farr, M. and Halliwell, B. (1984). Lipid peroxidation in rheumatoid arthritis thiobarbituric acid reactive material and catalytic iron salts in synovial fluid from rheumatoid patients. Clin. Sci. 66, 691-695. 

Quinlan, G.J., Evans, T.W. and Gutteridge, J.M.C. (1994). Linoleic acid and protein thiol changes suggestive of oxidative damage in the plasma of patients with adult respiratory distress syndrome. Free Bad. Res. Commun. 20, 299-306. 

The heart has a relatively low catalase activity, which, together with the superoxide dismutase (SOD) system, acts to remove hydrogen peroxide and superoxide radicals. In addition, in man, dietary vitamin C plays an important role in the reduction of vitamin E, an intrinsic antioxidant component of biological membranes (Chen and Thacker, 1986 Niki, 1987). Both vitamins C and E can also react directly with hydroxyl and superoxide radicals (HalliwcU and Gutteridge, 1989 Meister, 1992). 

During ischaemia, the activity of cellular antioxidant systems may be reduced (Ferrari et al. 1985 GaUnanes etal. 1992). In addition, a number of cellular pathways that produce free radicals are primed during ischaemia such as the xanthine/xanthine oxidase system (McCord, 1987), catecholamine auto-oxidation (Jackson et al., 1986) and the arachadonic acid pathway (Halliwell and Gutteridge, 1989). Thus, during early reperfusion there is a burst of free radical production (see Fig. 4.1) that may overwhelm the antioxidant systems of the cells. 

Gutteridge, J.M.C., Richmond, R, and HaUiweU, B. (1979). Inhibition of the iron-catalysed formation of hydroxyl radicals from superoxide and of lipid peroxidation by desferrioxamine. Biochem. J. 184, 469-472. 

It has long been recognized that ascorbate levels are low in patients with RA (Lunec and Blake, 1985) and ascorbate is predominantly found in the dehydro form. The presence of increased dehydroascorbate has been suggested to indicate its rapid oxidation by stimulated PMNs (Halliwell and Gutteridge, 1990). When ascorbate concentrations are lower than about 20 /tmol/1, as can occur in rheumatoid synovial fluid, the Fe(III) reducing effects of ascorbate outweigh its radical-scavenging effects. Ascorbate then causes increased OH formation and promotes lipid peroxidation (Blake et al., 1981). 

Gutteridge, J.M.C. (1986). Antioxidant properties of the proteins caeruloplasmin, albumin and transferrin. A study of their activity in serum and synovial fluid fiom patients with rheumatoid arthritis. Biochim. Biophys. Acta 869, 119-127. 

Halliwell, B. and Gutteridge, J.M.G. (1985). Importance of free radicals and catalytic metal ions in human disease. Mol. Aspects Med. 8, 89-193. 

Winyard, P.G., Blake, D.R., Chirco, S., Gutteridge, J.M.C. and Lunec, J. (1987a). Mechanism of exacerbation of rheumatoid synovitis by total-dose iron-dextran infusion in vivo demonstration of iron-promoted oxidant stress. Lancet i, 69-72. 

Gutteridge, J.M.C. and Smith, A. (1988). Anti-oxidant protection by haemopexin of haem-stimulated lipid peroxidation. Biochem. J. 256, 861-865. 

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