mice ( Figure 2 E ); (2) after APAP intoxication GSH concentrations were significantly lower in the Nlrp6 -/- than in the WT mice, although the difference was quite small ( Figure 2 E ); and (3) Nlrp6 -/- mice showed higher APAP GSH adduct levels after APAP administration; however, this difference did not reach statistical significance ( Figure 2 E ).
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Nlrp6 -/- mice on ABx even showed a trend toward lower liver injury as evidenced by GLDH and a lower liver-to-bodyweight ratio ( Figure 10 I and J ).
The differences in APAP metabolism were studied between WT and Nlrp6 -/- livers; we measured APAP and its metabolites in the systemic circulation before as well as 30 minutes after APAP intoxication and saw the following constellation: (1) no statistically significant difference in basal glutathione (GSH) concentrations was found between Nlrp6 -/- and WT mice, although a nonsignificant trend toward higher GSH was seen in the Nlrp6 -/- mice ( Figure 2 E ); (2) after APAP intoxication GSH concentrations were significantly lower in the Nlrp6 -/- than in the WT mice, although the difference was quite small ( Figure 2 E ); and (3) Nlrp6 -/- mice showed higher APAP GSH adduct levels after APAP administration; however, this difference did not reach statistical significance ( Figure 2 E ).