**Author details**

Ellen Friday

36 Dehydrogenases

both GDH and NHE in cell survival[26].

presumably reflecting both TRO's "pull" action and PIO's PPARγ- mediated downregulation of NHE gene expression. Significantly, the dual effect of glitazones to increase GDH flux while reducing NHE activity decreases proliferation(NHE) but increases cell survival(GDH) resulting in only a slight decrease in cell number[26]. Nor does adding troglitazone to glucose deleted cells induce massive cell death since the effect on GDH flux is additive (further reducing TCA intermediates and cell pH, **Figure 2**) and although proliferative rates are decreased, survival is enhanced [26]. Under these conditions, e.g. cell survival mechanisms, inhibition of GDH is most effective in causing massive cell death as occurs with the GDH inhibitor EGCG [5] combined with troglitazone [26]. Although rescue of cells is partly possible by restoring anaplerosis with methyl pyruvate, failure to restore NHE activity and the cellular acidosis preclude full recovery underlining the importance of

**Figure 5. Ammonium production from amino nitrogen of glutamine.** Cells were incubated for 18 hours in [2-15N] glutamine. TRO was used at 20 uM, PIO 10 uM. Results are from 3 experiments.

*Department of Medicine- Feist- Weiller Cancer Center Department of Cellular and Molecular Physiology, Louisiana State University Health Sciences Center, Shreveport, LA, USA* 

Robert Oliver III and Tomas Welbourne *Department of Cellular and Molecular Physiology, Louisiana State University Health Sciences Center, Shreveport, LA, USA* 

Fancesco Turturro *Department of Lymphoma; Myeloma, MD Anderson Cancer Center, Houston, TX, USA* 
