Bialas 2018 Int J Chron Obstruct Pulmon Dis
|Białas AJ, Siewiera K, Watała C, Rybicka A, Grobelski B, Kośmider L, Kurek J, Miłkowska-Dymanowska J, Piotrowski WJ, Górski P (2018) Mitochondrial functioning abnormalities observed in blood platelets of chronic smoke-exposed guinea pigs – a pilot study. Int J Chron Obstruct Pulmon Dis 13:3707—17 .|
Abstract: COPD represents a major global health issue, which is often accompanied by cardiovascular diseases. A considerable body of evidence suggests that cardiovascular risk is elevated by the activation of blood platelets, which in turn is exacerbated by inflammation. As reactive oxygen species are believed to be an important factor in platelet metabolism and functioning, the aim of our study was to perform a complex assessment of mitochondrial function in platelets in chronic smoke exposed animals with COPD-like lung lesions.
Eight-week-old, male Dunkin Hartley guinea pigs (the study group) were exposed to the cigarette smoke from commercial unfiltered cigarettes (0.9 mg/cig of nicotine content) or to the air without cigarette smoke (control group), using the Candela Constructions® exposure system. The animals were exposed for 4 hours daily, 5 days a week, with 2×70 mL puff/minute, until signs of dyspnea were observed. The animals were bled, and isolated platelets were used to monitor blood platelet respiration. The mitochondrial respiratory parameters of the platelets were monitored in vitro based on continuous recording of oxygen consumption by high-resolution respirometry.
An elevated respiration trend was observed in the LEAK-state (adjusted for number of platelets) in the smoke-exposed animals: 6.75 (5.09) vs 2.53 (1.28) (pmol O2/[s · 1×108 platelets]); bootstrap-boosted P1α=0.04. The study group also demonstrated lowered respiration in the ET-state (normalized for protein content): 12.31 (4.84) vs 16.48 (1.72) (pmol O2/[s · mg of protein]); bootstrap-boosted P1α=0.049.
Our results suggest increased proton and electron leak and decreased electron transfer system capacity in platelets from chronic smoke-exposed animals. These observations may also indicate that platelets play an important role in the pathobiology of COPD and its comorbidities and may serve as a background for possible therapeutic targeting. However, these preliminary outcomes should be further validated in studies based on larger samples. • Keywords: Mitochondria, Electron leak, Proton leak, Electron transport chain, ETC, Chronic obstructive pulmonary disease, COPD, Animal model • Bioblast editor: Plangger M • O2k-Network Lab: PL Lodz Watala C
Labels: MiParea: Respiration Pathology: COPD
Organism: Guinea pig Tissue;cell: Platelet Preparation: Intact cells
Coupling state: LEAK, ROUTINE, ET Pathway: ROX HRR: Oxygraph-2k