Expression of intracellular biochemical defects of lymphocytes in aging: proposal of a general aging mechanism which is not cell-specific.
There is a decline in immune capacity with age which is expressed on the organismic level by association with numerous immune-related diseases, on the cellular level by impaired mitogenesis, on the biochemical level by impaired metabolic pathways, and on the molecular level by decreased protein synthesis and degradation. Defects in various cofactors such as calcium and several nucleotides also occur and may be related to the impaired enzyme function during mitogenesis in the aged. The central cause for decreased mitogenesis in the aged could be a decrease in protein synthesis which appears to cause impaired enzyme induction. This impaired enzyme induction accounts in part for the decreased glycolytic flux and DNA synthesis in these cells. Decreased protein synthesis also has been associated with a decreased synthesis of lymphokines which help these cells to proliferate. Numerous other intracellular age-related defects of lymphocytes also occur which may collectively play important interdependent roles in the impaired lymphocyte function of the aged. A potential general underlying mechanism of cellular senescence is proposed based on a genetic "slowing-cycle" effect of transcription, translation, and enzyme induction with immunosenescence presented as an example of an expression of these basic defects.
D000375:Aging / Q000097:blood*; D006801:Humans; D008214:Lymphocytes / Q000378:metabolism*