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. 2023 Jan 2;59:102600. doi: 10.1016/j.redox.2023.102600

Fig. 1.

Fig. 1

Time-resolved metabolomics of human and mouse brain during normoxia and in response to warm ischemia ex vivo. (A) Succinate accumulation quantified by LC-MS/MS in mouse and human brain. Data are mean ± SEM. n = 4–8 human, n = 4 mice. (B) Venn diagram of the distinct metabolites detected by LC-MS in normoxic mouse and human brain. Metabolites are listed in Supplemental Tables 2 and 3(C) Changes in energy metabolism during warm ischemia ex vivo for human and mouse brain samples determined by LC-MS. Data are from Supplemental Tables 2 and 3 ATP, ADP and lactate are shown as Log2 Fold Change (FC) of metabolite intensity measured as peak areas (PA) for that sample. For the ratio of NADH and NAD PAs, the data show the ratio in these values determined for each sample. Note that the ratio of NADH and NAD+ PAs is related to but is not the same as the NADH/NAD+ molar ratio. Data are mean ± SEM. n = 4–8 human, n = 4 mice. (D) Venn diagrams showing the distinct metabolites detected in the mouse and human brain samples over different durations of ex vivo warm ischemia. Metabolites are listed in Supplemental Tables 2 and 3(E) PCA analysis of the changes in levels of metabolites during ex vivo warm ischemia for mouse and human brain samples. Metabolites are listed in Supplemental Tables 2 and 3