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. Author manuscript; available in PMC: 2010 Jul 1.
Published in final edited form as: Toxicol Appl Pharmacol. 2009 May 3;238(1):90–99. doi: 10.1016/j.taap.2009.04.019

Figure 4. Model optimization.

Figure 4

Model fitness status showed that DCA measurements were not supported by model B, in which the source of DCA formation was TCA only. (A) Model A for TCE → DCA, (B) Model B for TCA → DCA, (C) Model C for TCE+TCA → DCA, and (D) Model D for TCE → DCA (two-compartment). Filled circle, symbol and error bars represent mean of three replicates (animals) and standard deviation of each TCE metabolite at a given time point.