Fig. 5
From: Urban air particulate matter induces mitochondrial dysfunction in human olfactory mucosal cells
Exposure to PM increased mitochondrial ROS and altered key mitochondrial functions. a Mitochondrial ROS levels were quantified by MitoSOX labelling after 4 h exposure revealed a significant increase in cells exposed to PM2.5–1 and PM10–2.5 . b Significant loss of mitochondrial membrane potential was observed in all PM size classes. c Line plot displaying oxygen consumption rate (OCR) of hOM cultures exposed to PM and quantified in pmol/minute/μg after the addition of oligomycin (Olig), FCCP and Rotenone/Antimycin (Rot+Ant). d Basal respiration in cells exposed to PM1–0.2 (5.17 ± 0.59), PM2.5–1 (2.92 ± 1.03) and PM10–2.5 (2.32 ± 1.29), compared to the vehicle (4.44 ± 0.28). e Maximal respiration after exposure to PM1–0.2 (10.74 ± 0.26), PM2.5–1 (5.14 ± 0.86) and PM10–2.5 (4.96 ± 2.3), compared to the vehicle (11.01 ± 1.08). f Non-mitochondrial respiration after exposure to PM1–0.2 (1.38 ± 0.35), PM2.5–1 (1.86 ± 0.12) or PM10–2.5 (1.65 ± 0.25), compared to the vehicle (3.35 ± 0.16). g ATP production in hOM cells exposed for 24 h to PM1–0.2 (4.17 ± 0.72), PM2.5–1 (1.81 ± 0.01) or PM10–2.5 (1.1 ± 0.58), compared to the vehicle (3.47 ± 0.19). h Intracellular ATP levels reflected little variation in hOM cultures exposed to PM1–0.2 (0.28 μM ± 0.02 μM), PM2.5–1 (0.2 μM ± 0.04 μM) or PM10–2.5 (0.28 μM ± 0.13 μM) from vehicle control (0.31 μM ± 0.04 μM). The OCR was normalised by protein levels. * p < 0.05, **p < 0.01. n = four donors/group