Cannon 2016 Lung: Difference between revisions
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{{Publication | {{Publication | ||
|title=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. Β | |title=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. | ||
|info=[http://www.ncbi.nlm.nih.gov/pubmed/26899624 PMID: 26899624] | |info=[http://www.ncbi.nlm.nih.gov/pubmed/26899624 PMID: 26899624] | ||
|authors=Cannon DT, Liu J, Sakurai R, Rossiter HB, Rehan VK | |authors=Cannon DT, Liu J, Sakurai R, Rossiter HB, Rehan VK | ||
|year=2016 | |year=2016 | ||
|journal=Lung | |journal=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 O<sub>2< | |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 O<sub>2</sub> 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. | ||
|mipnetlab=US CA San Diego Cannon DT, US CA Torrance Rossiter HB | |||
}} | }} | ||
{{Labeling | {{Labeling | ||
| Line 11: | Line 12: | ||
|organism=Rat | |organism=Rat | ||
|tissues=Lung;gill | |tissues=Lung;gill | ||
|couplingstates=OXPHOS | |preparations=Permeabilized tissue | ||
|couplingstates=LEAK, OXPHOS, ET | |||
|pathways=N, S, CIV, NS | |||
|instruments=Oxygraph-2k | |instruments=Oxygraph-2k | ||
|additional= | |additional=2016-03 | ||
}} | }} | ||
Latest revision as of 12:00, 28 March 2018
| 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.
β’ O2k-Network Lab: US CA San Diego Cannon DT, US CA Torrance Rossiter HB
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
