The Effects of Storage and Ageing of Human Blood on the Levels of Asymmetric Dimethylarginine, and an Analysis of its Protein Source in Erythrocytes
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Nitric oxide (NO) is a vasodilator produced from arginine via the enzyme nitric oxide synthase (NOS). An endogenous inhibitor of NOS is asymmetric dimethylarginine (ADMA). ADMA is a protein metabolite that is produced from the post-translational methylation of the arginine residues in proteins. When these proteins are degraded into their amino acids, ADMA is released into blood. If levels of ADMA increase above physiologically normal levels, the resulting suppression of NO levels can lead to complications within the vascular system, such as athereogenesis and cardiovascular disease. ADMA levels can become elevated through stress to the system and aging of blood. This study investigated the accumulation of ADMA in ageing, stored human blood, and the protein source from which ADMA is released. It was hypothesized that ADMA would accumulate over time in the stored blood from the hospital blood blank and peak at 42 days when banked blood is normally discarded. Furthermore, it was proposed that hemoglobin was the main blood protein responsible for the release of ADMA, as it is the most abundant protein in red blood cells. The data from this study suggested that ADMA levels rapidly accumulated in stored blood up to 28 days of age, after which time the rate of accumulation in levels slowed. Using a ghost preparation and subsequent Western blot analysis, this study suggested that the blood protein spectrin might instead be a source of ADMA. Elevated levels of ADMA are responsible for many vascular diseases and therefore further research on this protein metabolite should occur so that banked blood can be used safely.