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. Author manuscript; available in PMC: 2022 Nov 1.
Published in final edited form as: Free Radic Biol Med. 2021 Aug 26;175:18–27. doi: 10.1016/j.freeradbiomed.2021.08.232

Fig. 4. Stimulation of mitochondrial ROS and depletion of mitochondrial lipids in PCBP1Δhep mice.

Fig. 4.

A. Elevated ROS production in hepatocytes from PCBP1Δhep mice. Primary hepatocytes were analyzed for mitochondrial ROS using mitochondrial-specific ROS probe Mitosox. Fluorescence expressed as ratio to mitotracker green to normalize for mitochondrial content. Quantification of fluorescence intensity ratios at right. Analyses were repeated thrice; 25–40 cells were analyzed in each experiment. B. Elevated mRNA levels of mitochondrial ROS marker UCP2 in PCBP1Δhep livers. C. Depletion of Coenzyme Q and major cardiolipins in PCBP1Δhep livers. Global lipid analysis of livers was performed. Predominant cardiolipin, tetralinoleoyl (C18:2)4 cardiolipin is shown. Acylcarnitine, a lipid carrier and marker of impaired mitochondrial lipid metabolism, at right. Data represent mean ± SD. (A,B)* indicates p < 0.05, **p < 0.002 as determined by unpaired t-test. (C) * indicates q < 0.05, ** indicates q < 0.002 as determined by False Discovery Rate (FDR) determined using the two-stage linear step-up procedure of Benjamini, Krieger and Yekutieli, with Q = 5%.