Advanced glycation end products formation

Table 7.4 Inhibitory concentration 50% (IC50) of advanced glycation end product formation by pure ginsenosides and an Ontario ginseng extract (n = 3)...

Wirasathien L, Pengsuparp T, Suttisri R, Ueda H, Moriyasu M, Kawanishi K. (2007) Inhibitors of aldose reductase and advanced glycation end-products formation from the leaves of Stelechocarpus cauliflorus R.E. Er. Phytomedicine 14 546-550. 

Y. Al-Abed, T. Mitsuhashi, H. Li, J. A. Lawson, G. A. FitzGerald, H. Founds, T. Donnelly, A. Cerami, P. Ulrich, and R. Bucala, Inhibition of advanced glycation end product formation by acetaldehyde Role in the cardioprotective effect of ethanol, Proc. Natl. Acad. Sci. USA, 1999, 96, 2385-2390. 

Tilton RG, Chang K, Hasan KS, et al. Prevention of diabetic vascular dysfunction by guanidines. Inhibition of nitric oxide synthase versus advanced glycation end-product formation. Diabetes 1993 42 221-232. 

Jang DS, Lee GY, Lee YM, Kim YS, Sun H, Kim DH, Kim JS. (2009) Flavan-3-ols having a y-Lactam from the roots of Actinidia arguta inhibit the formation of advanced glycation end products in vitro. Chem Pharm Bull 57 397-400. 

FIGURE 3.3 Schematic showing possible sites of intervention by carnosine during formation of cross-linked methylglyoxal-modified proteins. AGE, advanced glycation end-product. 

Alhamdani, M. S. S., Al-Azzawie, H. F., and Abbas, F. K. (2007b). Decreased formation of advanced glycation end-products in peritoneal fluid by carnosine and related peptides. Perit. Dial. Int. 27, 86-89. 

Cantero, A. V., Portero-Otin, M., Ayala, V., Auge, N., Sanson, M., Elbaz, M., Thiers, J. C., Pamplona, R., Salvayre, R., and Negre-Salvayre, A. (2007). Methylglyoxal induces advanced glycation end product (ages) formation and dysfunction of PDGF receptor-beta Implications for diabetic atherosclerosis. FASEB J. 21,3096-3106. 

The impairment of glucose utilization could result from the modification of the glycolytic enzymes under oxidative stress effects. Oxidative stress is an important factor leading to the pathophysiologcal alterations in conformational diseases. Oxidative stress is manifested in protein oxidation, lipid peroxidation, DNA oxidation, and advanced glycation end-products, as well as reactive oxygen species (ROS), and reactive nitrogen species (RNS) formation. Either the oxidants or the products of oxidative stress could modify the proteins or activate other pathways that may lead to additional impairment of cellular functions and to neuronal loss [57, 58]. 

A. A. Booth, R. G. Khalifa, P. Todd, and B. G. Hudson, In vitro kinetic studies of formation of antigenic advanced glycation end products (AGEs). Novel inhibition of post-Amadori glycation pathways, J. Biol. Chem., 1997, 272, 5430-5437. 

Figure 1.11 Illustration of advanced glycation end-product (AGE) formation.

The assays most widely employed are the measurement of thiobarbituric acid-reactive species (TBARS) and the formation of conjugated dienes, markers of lipid peroxidation [31-33] the determination of advanced oxidation protein products (AOPP), a marker of protein oxidation, and of advanced glycation end-products (AGE) [34-37] the measurement of erythrocyte antioxidant potential [38]. Of particular importance is the isoprostanes determination, since these compounds are formed by the free radical catalysed peroxidation of arachidonic acid, which is independent of the cyclooxygenase enzyme, giving rise to stable compounds, measurable in urine [39]. As recently assessed in a Workshop on markers of oxidative damage and antioxidant protection [40], currently available methods for the determination of antioxidant and redox status are not yet generally suitable for routine clinical applications, essentially for the lack of standardized tests. 

Wu Q, Chen H, Lv Z, Li S, Hu B, Guan Y et al (2013) Oligomeric procyanidins of lotus seedpod inhibits the formation of advanced glycation end-products by scavenging reactive carbonyls. Food Chem 138 1493-1502... 

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