Steatotic livers are susceptible to normothermic ischemia-reperfusion injury from mitochondrial Complex-I dysfunction

Figure 4 Mitochondrial function of lean and steatotic livers subjected to sham or ischemia-reperfusion injury with or without ischemic preconditioning. Baseline MF was similar between lean and steatotic livers in all outcome measures. Lean-Sham and Steatotic-Sham had stable CI-OXPHOS (A, B), CII-OXPHOS (C, D), and RCR (E, F) throughout the procedure. CI-OXPHOS (A, B), CII-OXPHOS (C, D), and RCR (E, F) were significantly lower following 60 min of ischemia in Lean-IRI, Lean-IPC, Steatotic- IRI, and Steatotic-IPC livers compared to the corresponding sham group. Following reperfusion, CI-OXPHOS (B) and RCR (F) were significantly lower in Steatotic-IRI and Steatotic-IPC livers compared to Steatotic-Sham or lean livers, while CII-OXPHOS (D) returned to pre-ischemic levels comparable to Steatotic-Sham or lean livers (D). Data are shown as mean ± SE (n = 10 rat/group; Lean-Sham, open circle; Lean-IRI, open square; Lean-IPC, open triangle; Steatotic-Sham, closed circle; Steatotic-IRI, closed square; Steatotic-IPC, closed triangle). ^aP < 0.05 vs Lean-IRI; ^cP < 0.05 vs Lean-IPC (end of reperfusion). IRI: Ischemia-reperfusion injury; IPC: Ischemic preconditioning.