Retina protein damage

Proteasomal pathways degrade the oxidized and misfolded proteins. The partial loss of proteasomal expression and function has been described in the retinae of elderly rats (Louie et al., 2002). Oxidative and metabolic stress can have a cumulative effect. Accumulation of oxidatively damaged molecules can lead to the dysfunction of various metabolic and signaling pathways. 

The presence of covalently attached glucose residues generally causes a protein to malfunction. This has serious effects on the eye and the kidney. In the eye some of the proteins have slow turnover, such as crystalUns in the lens and structural proteins in the retina. In the kidney, structural proteins in cells and in the extracellular matrix are exposed to high concentrations of glucose from the blood and the urinary filtrate. Damage to these tissues leads to blindness, vascular disease with high blood pressure, and nephropathy, respectively. 

Evidence for the role of AGEs in vascular complications has been presented (1). There is increased concentration of AGE residues in tissue sites such as the renal glomeruli, retina, and peripheral nerve where vascular complications arise. Experimentally, the injection of AGE precursor, methyl glyoxal, or AGE-modified proteins, induces vascular damage similar to that seen in the diabetic condition. 

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