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Glucose radical

Figure 10. Illustrative mechanism for the reactions of the glucose radical formed by loss of hydrogen from the C-1 position final products are indicated. Reproduced from von Sontag [33] and WHO Technical Report No. 890 [43] with permission. Figure 10. Illustrative mechanism for the reactions of the glucose radical formed by loss of hydrogen from the C-1 position final products are indicated. Reproduced from von Sontag [33] and WHO Technical Report No. 890 [43] with permission.
Cation (Section 1 2) Positively charged ion Cellobiose (Section 25 14) A disacchande in which two glu cose units are joined by a 3(1 4) linkage Cellobiose is oh tamed by the hydrolysis of cellulose Cellulose (Section 25 15) A polysaccharide in which thou sands of glucose units are joined by 3(1 4) linkages Center of symmetry (Section 7 3) A point in the center of a structure located so that a line drawn from it to any element of the structure when extended an equal distance in the op posite direction encounters an identical element Benzene for example has a center of symmetry Cham reaction (Section 4 17) Reaction mechanism m which a sequence of individual steps repeats itself many times usu ally because a reactive intermediate consumed m one step is regenerated m a subsequent step The halogenation of alkanes is a chain reaction proceeding via free radical intermediates... [Pg.1278]

Decreased cerebral blood flow, resulting from acute arterial occlusion, reduces oxygen and glucose delivery to brain tissue with subsequent lactic acid production, blood-brain barrier breakdown, inflammation, sodium and calcium pump dysfunction, glutamate release, intracellular calcium influx, free-radical generation, and finally membrane and nucleic acid breakdown and cell death. The degree of cerebral blood flow reduction following arterial occlusion is not uniform. Tissue at the... [Pg.39]

Diabetic patients have reduced antioxidant defences and suffer from an increased risk of free radical-mediated diseases such as coronary heart disease. EC has a pronounced insulin-like effect on erythrocyte membrane-bound acetylcholinesterase in type II diabetic patients (Rizvi and Zaid, 2001). Tea polyphenols were shown to possess anti-diabetic activity and to be effective both in the prevention and treatment of diabetes (Choi et al, 1998 Yang et al, 1999). The main mechanism by which tea polyphenols appear to lower serum glucose levels is via the inhibition of the activity of the starch digesting enzyme, amylase. Tea inhibits both salivary and intestinal amylase, so that starch is broken down more slowly and the rise in serum glucose is thus reduced. In addition, tea may affect the intestinal absorption of glucose. [Pg.138]

Hunt, J. (1994). Glucose chemistry and atherosclerosis in diabetes mellitus. In Free Radicals in the Environment, Medicine and Toxicology. Current Aspects and Current Highlights (eds. H. Nohl, H. Esterbauer and C. Rice-Evans) pp. 137-162, Richelieu Press, London. [Pg.50]

Hunt, J.V., Dean, R.T. and Wolff, S. (1988). Hydroxyl radical production and autoxidative glycosylation. Glucose oxidation as the cause of protein damage in the experimental glycation model of diabetes mellitus and ageing. Biochem. J. 256, 205-212. [Pg.50]

Several studies have demonstrated the production of mucosal damage and/or increased mucosal permeability by hydrogen peroxide, the hydroxyl radical, or by installation of xanthine or glucose oxidase (Gregaard et al., 1982 Parks et al., 1984 Joubert-Smith et al., 1991 Kohen etal., 1992). [Pg.146]

It should be remembered that some of the established antioxidants have other metabolic roles apart from free-radical scavenging. The finding of reduced antioxidant defences in diabetes, for example, may not be prima fascie evidence of increased oxidative stress, since alternative explanations may operate. For example, this may reflect a response to reduced free-radical activity as su ested by the results of a previous study (Collier et al., 1988). In the case of ascorbate, an alternative explanation has been proposed by Davis etal. (1983), who demonstrated competitive inhibition of ascorbate uptake by glucose into human lymphocytes. This view is supported by the similar molecular structure of glucose and ascorbic acid (see Fig. 12.4) and by a report of an inverse relationship between glycaemic control and ascorbate concentrations in experimental diabetes in rats. Other investigators, however, have not demonstrated this relationship (Som etal., 1981 Sinclair etal., 1991). [Pg.187]

Under certain conditions, glucose can induce free-radical production... [Pg.188]

Glucose may auto-oxidize (like other alphahydroxy-aldehydes) and generate hydroxyl radicals in a transition-metal-catalysed reaction, and induce both fragmentation and conformational changes in glycated proteins (Hunt et al., 1990). [Pg.190]

Improving giycaemic control may not only reduce the rate of non-enzymatic glycosyiation and monosaccharide autooxidation, but lower polyol pathway activity. In addition, it should have a beneficial effect on other haemodynamic and hormonal factors involved in the development of diabetic vascular disease. However, in studies of diabetic retinopathy, rapid control of glucose levels by intensive insulin therapy has been shown to worsen vascular disease initially and it could be postulated that a sudden improvement in retinal blood flow promotes further free-radical damage as part of a reperfusion-ischaemic injury. [Pg.194]

Hunt, J.V., Smith, C.T. and WolflF, S.P. (1990). Autooxidative glycosylation and possible involvement of peroxides and free radicals in LDL modification by glucose. Diabetes 39, 1420-1424. [Pg.196]


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See also in sourсe #XX -- [ Pg.719 ]




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