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. 2023 May 25;13(5):e1276. doi: 10.1002/ctm2.1276

FIGURE 3.

FIGURE 3

Mitochondrial oxidative dysfunction in patients with alcohol‐associated hepatitis. Oxygen consumption measured using high‐sensitivity respirometry in peripheral blood mononuclear cells (PBMC) from healthy controls (HC), heavy drinking controls (HD), and patients with alcohol‐associated hepatitis (AH) in the same patient in intact and permeabilised cells (in the discovery cohort). (A) Intact cell responses in a discovery cohort including responses to ATP synthetase inhibitor‐oligomycin, uncoupler of oxidative phosphorylation, 2‐[2‐[4‐(trifluoromethoxy) phenyl]hydrazinylidene]‐propanedinitrile (FCCP), complex I inhibitor rotenone, and complex III inhibitor Antimycin A. Intact cell respiration, oxidative phosphorylation, proton leak, maximum respiration (Max.R.), and reserve respiratory capacity (R.R.). (HC, n = 12; HD, n = 6; AH, n = 12). (B) Intact cell responses in a validation cohort (HC, n = 7; AH, n = 10). (C) Oxygen consumption measured in permeabilised PBMC in the same validation cohort. Responses to Malate (M), Pyruvate (P), ADP (D), Glutamate (G), and Succinate (S), Max.R., Complex II, R.R., rotenone‐insensitive/sensitive, and Complex IV respiration. Mean ± SD *p < .05; **p < .01; ***p < .001. AH Alcohol‐associated hepatitis; HC healthy control; HD heavy drinkers with no liver disease.