Cannon 2016 Lung
| Cannon DT, Liu J, Sakurai R, Rossiter HB, Rehan VK (2016) Impaired lung mitochondrial respiration following perinatal nicotine exposure in rats. Lung 194:325-8. |
Cannon DT, Liu J, Sakurai R, Rossiter HB, Rehan VK (2016) Lung
Abstract: Perinatal smoke/nicotine exposure predisposes to chronic lung disease and morbidity. Mitochondrial abnormalities may contribute as the PPARΞ³ pathway is involved in structural and functional airway deficits after perinatal nicotine exposure. We hypothesized perinatal nicotine exposure results in lung mitochondrial dysfunction that can be rescued by rosiglitazone (RGZ; PPARΞ³ receptor agonist). Sprague-Dawley dams received placebo (CON), nicotine (NIC, 1 mg kg(-1)), or NIC + RGZ (3 mg kg(-1)) daily from embryonic day 6 to postnatal day 21. Parenchymal lung (~10 mg) was taken from adult male offspring for mitochondrial assessment in situ. ADP-stimulated O2 consumption was less in NIC and NIC + RGZ compared to CON (F[2,14] = 17.8; 4.5 Β± 0.8 and 4.1 Β± 1.4 vs. 8.8 Β± 2.5 pmol s mg(-1); p < 0.05). The respiratory control ratio for ADP, an index of mitochondrial coupling, was reduced in NIC and remediated in NIC + RGZ (F[2,14] = 3.8; p < 0.05). Reduced mitochondrial oxidative capacity and abnormal coupling were evident after perinatal nicotine exposure. RGZ improved mitochondrial function through tighter coupling of oxidative phosphorylation.
Labels: MiParea: Respiration, Exercise physiology;nutrition;life style, Pharmacology;toxicology
Organism: Rat
Tissue;cell: Lung;gill
Preparation: Permeabilized tissue
Coupling state: LEAK, OXPHOS, ET
Pathway: N, S, CIV, NS
HRR: Oxygraph-2k
2016-03
