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Fig. 2 | Molecular Medicine

Fig. 2

From: Metabolomics analysis elucidates unique influences on purine / pyrimidine metabolism by xanthine oxidoreductase inhibitors in a rat model of renal ischemia-reperfusion injury

Fig. 2

Purine nucleotide concentrations measured by HPLC. Concentrations of ATP, ADP, AMP, hypoxanthine, xanthine, and uric acid were measured by HPLC. In the stationary state, ATP and TAN levels were significantly higher in the Feb-S and Top-S groups than in the Veh-S and Allo-S groups (b, c), whereas xanthine was not detected (ND) in the Veh-S group, and uric acid levels decreased in the inhibitor-treated groups (g, h). ADP levels increased in the Feb-S and Top-S group compared with that in the Veh-S group (d). In the ischemic state, energy charge and concentrations of purine nucleotide decreased considerably from the stationary condition (a, b, c, d); hypoxanthine levels were higher, and xanthine and uric acid levels were lower in the inhibitor-treated groups (f, g, h). In the reperfused state, TAN and ATP levels were higher in the Feb-R group than in the Veh-R group (B, C); hypoxanthine and xanthine remained positive only in inhibitor-treated groups (f, g), and uric acid in Veh-R rats returned to the stationary level (h). Energy charge and TAN were calculated as follows: energy charge = ATP + 0.5*ADP/ATP + ADP + AMP, TAN = ATP + ADP + AMP. Concentrations are expressed as nmol/g wet weight; the data are presented as the mean ± SEM (n = 5~6). *P < 0.05 and **P < 0.01 versus Veh; #P < 0.05 and ##P < 0.01 versus Allo; one-way ANOVA followed by Games–Howell’s test

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