Plasma proteins, damage detection

Not all data confirm accumulation of protein oxidation products with age. For example, comparison of 9-month-old and 24-month-old female Long-Evans/Wistar hybrid rats did not demonstrate any age-related increase of o-tyrosine and 3-nitrotyrosine in the heart, skeletal muscle, and liver. These observations were interpreted as indications suggesting that proteins damaged by the hydroxyl radical and reactive nitrogen species did not accumulate in these tissues with advancing age (L7). Dityrosine could not be detected in human plasma proteins or haemoglobin (with the detection limit of 1 pmol/mg protein) (D3), but may accumulate in... 

There is evidence of an increase in the redox-active fraction of plasma Cu in human aging [54]. This arises because of the apparent increase in the proportion of an oxidized form of ceruloplasmin, an antioxidant ferroxidase that carries > 90% of total plasma Cu. The damaged ceruloplasmin allows the Cu it binds (6 moles per protein unit) to become EPR-detectable [54]. This is an example of how damage to a cuproprotein may unleash abnormal redox chemistry, a principle that we believe underhes the pathology of AD. 

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