Cellular life span

Kletsas, D., Pratsinis, H., Gioni, V., Pilichos, K., Yiacoumettis, A. M., and Tsagarakis, S. (2007). Prior chronic in vivo glucocorticoid excess leads to an anabolic phenotype and an extension of cellular life span of skin fibroblasts in vitro. Ann. N. Y. Acad. Sci. 1100, 449-454. 

Umezaki, R., Murai, K., Kino-oka, M. and Taya, M. (2002) Correlation of cellular life span with growth parameters observed in successive cultures of human keratinocytes. J. Biosci. Bioeng., 94, 231-236. 

Kondoh, H. (2008). Cellular life span and the Warburg effect. Exp Cell Res 314(9), 1923-1928. 

The cellular elements of the blood have a short life span and must be continuously replaced. The formation of red blood cells, white blood cells, and platelets, collectively, is referred to as hematopoiesis. This process takes place in the red bone marrow. In adults, red bone marrow is found in the pelvis, ribs, and sternum. 

The generation of free radicals in mammalian cells is continuous and occurs as a result of both normal and abnormal cellular activity and also environmental perturbations. It has been estimated that every single one of our body s cells suffers approximately 10,000 free radical hits per day. Over a typical 70-year life span, the body generates an estimated 17 tons of free radicals. DNA is a probable target, which may partially explain the higher frequency of mutations in the elderly. In addition to DNA, cell membranes, proteins, and fats are also being targeted by free radicals. 

Platelets isolated under the experimental conditions described here are remarkably consistent in their responses to stimuli. The normal laboratory life span for such a cell preparation is 6-7 hr at room temperature. This time frame is sufficiently broad enough to allow meaningful experiments to be done on the turnover of cellular phospholipids under a variety of experimental conditions. 

Primary cultures of cerebromicrovascular endothelial cells (CEC) derived from rat, bovine, porcine, mouse and human can rapidly lose key phenotypic markers of the blood-brain barrier (BBB) and undergo cellular senescence after a limited number of divisions in vitro. Furthermore, expression of BBB markers varies considerably among BCEC obtained from different species. These issues, compounded with the problems associated with very limited availability of human brain biopsies, small initial yield of cells and short proliferative life span of human cells, greatly restrict the utility of primary human BCEC as a reliable in vitro BBB model. Therefore, Muruganandam et al. (1997) developed an immortalized human cerebromicrovascular endothelial cell line as an in vitro model of the human blood-brain barrier. 

Reactive oxygen species are produced by the respiration cycle and metabolic activity. Quantifying reactive oxygen species is difficult because of their short life span, low concentrations, and the existence of cellular scavenging systems (Dufour and Larsson, 2004). 

Cell tines offer several advantages over primary cell cultures, such as an unlimited life-span and the lack of time-consuming isolation procedures. Additionally once established, they are often more stable than primary cells which are usually in a continuous state of de-differentiation. Thus, the majority of in vitro nephrotoxicity studies have been performed on renal epithelial cell tines. In normal somatic cells, telomeres, the tandemly repeated hexamers at the end of mammalian chromosomes, act as the cellular replicative clock [43] and shorten at each cell division. Once telomeres have exceeded a certain critical length, the so called "Hayflick limit" [44], the cell enters replicative senescence and no longer proliferates. Until recently the most widely used renal cell tines were those which arose from spontaneously acquired immortalization in culture. These cell tines include LLC-PK (Hampshire pig) [45,46], JTC-12 (cynomolgus monkey) [47] and OK (American opossum) [48] cells, which exhibit biochemical and antigenic characteristics suggestive of proximal... 

Pyruvate Idnase deficiency (OMIM 266200) is the most common cause of nonspherocytic hemolytic anemia due to defective glycolysis. The allelic frequency is estimated to be around 2%. The consequent lack of sufficient energy, which is required for normal functioning and cellular survival, shortens the life span of the mature PK-deficient erythrocyte. Consequently, PK-deficient patients display a phenotype of nonspherocytic hemolytic anemia albeit with variable clinical severity. The clinical symptoms vary from neonatal death to a well-compensated hemolytic anemia. Patients benefit in general from a splenectomy. Pyruvate kinase deficiency is transmitted as an autosomal recessive disease. To date, more than 130 mutations in PKLR have been reported to be associated with pyruvate kinase deficiency (see Figure 21-10 for overview see reference 221). Most (70%) of these mutations are missense mutations affecting conserved residues in structurally and functionally important domains of PK. Splice site mutations, a deletion. 

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