Intracellular myoblastic cell

Fig. 3 Relationship between ATP depletion and Pgp expression levels in various cells. The studies included human breast carcinoma cells, MCF-7, and their MDR subline, MCF-7/ADR human oral epidermoid carcinoma cells, KB, and their MDR subline, KBv wUd-type porcine kidney epithelial cells, LLC-PKl, and human MDRl-transfected cells, LLC-MDRl human umbilical vein endothelial cells, HUVEC bovine brain microvessel endothelial cells, BBMEC and murine myoblast cells, C2C12. EC50 values for each of the cell lines were determined from the dose response curves as the concentration of Plutonic P85 inducing a 50% decrease in intracellular ATP following 2 h exposure of the cells to the block copolymer. The drug efflux transport proteins were identified using the im-munoblot technique and normalized to constitutively expressed y3-actin. Plotted using data reported in [33]...

As noted earlier, glial cells are a potentially important component of the blood-brain barrier. In our laboratory, we are investigating the uptake of thyroid hormone into cultured cells as models of intracellular uptake in the CNS, and we have included a human glioma cell line in these studies. We have also made a point of looking at the uptake of T as well as T3 since the major source of intracellular T3 in nerve cells is from monodeiodination of T after it is taken into the cell. In the glioma cells as well as in human and mouse neuroblastoma cells and human medulloblastoma cells, specific transport of thyroid hormones can be demonstrated at the plasma membrane. Thus, nervous system cells share this property with hepatocytes, skeletal myoblasts and several other cell types that have been investigated ... 

We propose that conditions altering the availability of NAD may be signaled to chromatin by the intermediacy of poly(ADP-ribose) (Fig. 2). The question is whether this signal operates imder physiological conditions. Some reports have provided direct evidence that NAD- depletion forced upon cells by incubation in nicotinamide-free medium, arrests poly(ADP-ribose) synthesis (5) and drastically alters chromatin functions (5-7). For example, DNA repair in response to a chemical carcinogen was arrested under these conditions, but could be reestablished with nicotinamide, which restored normal intracellular NAD- and poly(ADP-ribose) levels (5). Similarly, myoblast differentiation was reversibly inhibited either by nicotinamide starvation or by selective inhibition of poly(ADP-ribose) polymerase (7). These results illustrate that nutritional manipulation of... 

---