| Popis: |
The growth of human diploid fibroblast-like cells (HDF) in culture can be inhibited by reducing the level of extracellular Ca2+ in the incubation medium (1). The mechanism(s) by which lowered extracellular Ca2+ inhibits the growth of HDF is unclear. Certain evidence, however, indicates that it is the result of complex alterations in the Ca2+ pools, involving both the mobilization of intracellular stores and plasma membrane transport (2, 3). Mono(ADP-ribosyl) transfer reactions have been implicated in both of these processes (4, 5). Additionally, certain studies have provided evidence for the involvement of GTP-binding proteins (G-proteins) in the regulation of Ca2+ mobilization (6); and others have linked the regulation of G-protein function to mono(ADP-ribosyl)ation catalyzed by bacteria toxins (5, 7, 8). The present studies were undertaken to determine if extracellular Ca2+ depletion of HDF affects cellular NAD metabolism. A lowering of NAD pools in the absence of altered NAD biosynthesis would suggest a relationship between the effects of Ca2+ depletion and ADP-ribosylation reactions since they are NAD consuming processes. |
