Evaluation of advanced glycation end-products in diabetic and inherited canine cataracts

Abstract

RAGE and PCNA expression did not increase with cataractogenesis, possibly due to overexpression associated with normal aging and constant exposure to oxidative stress from sunlight-related ultraviolet irradiation, respectively. However, p21 and PCNA increased in diabetic cataractogenesis suggesting cell cycle and proliferation dysregulation. This may be related to the rapid onset in this type of cataract compared with the more chronic and slower-to-develop inherited cataracts.

Antiglycation Effects of Carnosine and Other Compounds on the Long-Term Survival of Escherichia coli

“…Specifically, we found that both folic acid and aminoguanidine each displayed some protective capacity against glucose and/or MG-related toxicity. Other compounds tested that did not show protection in these assays included green tea extract, S-lactoyl glutathione, and B vitamins B 1 , B 6 , and B 12 .…”

“…The principal mechanisms of glycation-related damage involve cross-links between proteins and/or DNA, modifying or destroying their functional properties (2,8,38). Most studies of glycation have been performed with eukaryotes because of its relationship to aging and disorders such as Alzheimer's disease and diabetes (6,21,30,42). However, several studies (32,33) have shown that glycation also takes place in Escherichia coli, affecting protein and DNA of this prokaryote.…”

The effect of steam pelleting of a dry dog food on the Maillard reaction

“…Their endogenous analogues, advanced glycation end-products (AGE), as well as dietary MRPs have been associated with the etiology of age-related diseases in humans, such as diabetes mellitus and impaired renal function (Singh et al, 2001). In dogs, elevated levels of AGEs in tissue proteins were observed in a number of diseases with increasing age (Bras et al, 2007;Comazzi et al, 2008;Shapiro et al, 2008;Chiers et al, 2010) and it is possible that bioavailable dietary MRPs contribute to the endogenous AGE levels in dogs as has been reported for humans (Koschinsky et al, 1997;Uribarri et al, 2005).…”

Lens epithelial cell apoptosis initiates diabetic cataractogenesis in the Zucker diabetic fatty rat

“…Diabetic cataracts have elevated Amadori products and AGEs when compared to normal lenses [49]. The receptor for AGEs (RAGE) increases in the human cataract, and should correlate with increased DNA damage of LECs [50]. The expression of RAGE protein and mRNA was increased by the RAGE-specific ligand S100b [51].…”