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J M Gutteridge

Publications and source records attributed to J M Gutteridge.

222 records · Page 13Linked to original sources

Age pigments: role of iron and copper salts in the formation of fluorescent lipid complexes.

Free radicals which abstract hydrogen atoms from unsaturated fatty acids initiate lipid autoxidation. Transition metal ions, however, usually stimulate lipid autoxidation by decomposing peroxides to release active radicals which can then initiate further autoxidation. Lipid peroxides produced in vivo, both enzymically and non-enzymically, are probably decomposed in this way resulting in the formation of fluorescent lipid complexes. The role of iron and copper salts in their formation has been studied using sequential techniques on fatty acid and phospholipid preparations.

Animals↗

Carminic acid-promoted oxygen radical damage to lipid and carbohydrate.

The food colouring carminic acid redox cycles to produce free radicals. These radicals, in the presence of trace amounts of iron salts, readily damage membrane lipid and degrade the carbohydrate deoxyribose. Damage to membrane lipid appears to involve mainly organic oxygen radicals such as alkoxy and peroxy radicals, whereas that to deoxyribose implicates the hydroxyl radical formed in a Fenton-type reaction. Antioxidants and iron chelators prevent such damage.

Animals↗

Sequential oxidative damage, and changes in iron-binding and iron-oxidising plasma antioxidants during cardiopulmonary bypass surgery.

Cardiopulmonary bypass patients undergoing heart valve replacement surgery appear to be under oxidative stress, when compared with normal healthy controls, by showing increased levels of protein and lipid damage. During bypass surgery two further episodes of oxidative stress occur. The first is seen when patients are placed on extracorporeal blood circulation and oxygenation which results in a rise in lipid peroxides and thiobarbituric acid-reactive substances. The second phase of oxidative stress occurs during reperfusion of the myocardium following removal of the aortic cross clamp. Coincident with evidence of increased oxidative damage to lipids during these latter phases of oxidative stress were decreases in plasma iron-binding and iron-oxidising antioxidant activities.

Antioxidants↗

Free radical damage to polyene antifungal antibiotics: changes in biological activity and thiobarbituric acid reactivity.

Polyene antifungal antibiotics contain thiobarbituric acid-reactive substances suggestive of the presence of peroxidic compounds. These peroxides appear to play no part in the drug's antifungal activities. The polyenes were relatively stable to further oxidation in air, but lost biological activity and native ultraviolet absorption upon irradiation with ultraviolet light or incubation with iron salts. No evidence was found for the participation of hydroxyl radicals in the observed damage to the polyene molecules. However, organic oxygen radicals were implicated and protection against ferrous salt dependent damage could be afforded by the addition of the antioxidant propylgallate.

Air↗

Malondialdehyde formation from lipid peroxides in the thiobarbituric acid test: the role of lipid radicals, iron salts, and metal chelators.

Most of the chromogen formed when peroxidized material is heated with thiobarbituric acid (TBA) can be ascribed to a colored complex formed between malondialdehyde (MDA) and TBA. Even when little MDA is present, large amounts of MDA-TBA adduct can be formed. This is because lipid peroxides break down to release MDA during the test conditions. Iron is not essential for the breakdown of the peroxides but is essential for the formation of TBA reactivity. This can be related to the ability of iron to decompose lipid peroxides with the release of peroxy radicals, which are precursors of MDA. These peroxy radicals, when released, can initiate further peroxidation during the heating stage of the TBA test. Fatty acids in the absence of lipid peroxides do not undergo significant peroxidation during the acid-heating stage of the TBA test.

Chelating Agents↗