Sudden senescence syndrome plays a major role in cell culture proliferation (CROSBI ID 85843)
Prilog u časopisu | izvorni znanstveni rad | međunarodna recenzija
Podaci o odgovornosti
Rubelj, Ivica ; Huzak, Miljenko ; Brdar, Branko
engleski
Sudden senescence syndrome plays a major role in cell culture proliferation
Normal human cells of various types have a finite and predictable proliferative potential in vitro. This limited life span is due to a gradually increasing fraction of senescent cells that appear in the culture in sudden and stochastic fashion due to a phenomenon referred to as sudden senescence syndrome (SSS). Because nondividing cells increasingly accumulate in the culture, dividing cells have to compensate for nondividers in order to accomplish additional population doubling (PD). Thus, individual dividing cells undergo more divisions, called cell generations (CG), than the number of PDs.Based on integrated experimental data, we claculated maximum CG for normal human diploid fibroblasts (HDF). It appears that for HDF culture that undergo 65 PDs, a calculated final CG is at least 126. Based on obtained value for CG we calculated the total size of the culture, both with and without effects of SSS. If no SSS tages place and cells divide by geometrical progession, the culture will grow up to 2(126) or 10(38) cells. By constantly eliminating cells from further divisions, causing cell loss (CL), SSS reduces the total size of the culture at every point during its proliferation. Calculated value for CL is enormous, so that the culture of 10(38) cells is reduced to to only 10(19) cells, thus as little as 10(-17)% of its size! Accordingly, by preventing virtually every cell in the culture from reaching its maximum doubling capacity, SSS appears to be the most important mechanism that influence cell culture proliferation.
sudden senescence syndrome; aging; cell proliferation; cell senescence
nije evidentirano
nije evidentirano
nije evidentirano
nije evidentirano
nije evidentirano
nije evidentirano
Podaci o izdanju
112 (3)
2000.
233-241
objavljeno
0047-6374
1872-6216
10.1016/s0047-6374(99)00090-1
Povezanost rada
Matematika, Biologija