2011
DOI: 10.1007/s11064-011-0447-9
|View full text |Cite
|
Sign up to set email alerts
|

Cigarette Smoke Inhibits Brain Mitochondrial Adaptations of Exercised Mice

Abstract: Physical exercise and smoking are environmental factors that generally cause opposite health-promoting adaptations. Both physical exercise and smoking converge on mitochondrial adaptations in various tissues, including the pro-oxidant nervous system. Here, we analyzed the impact of cigarette smoking on exercise-induced brain mitochondrial adaptations in the hippocampus and pre-frontal cortex of adult mice. The animals were exposed to chronic cigarette smoke followed by 8 weeks of moderate-intensity physical ex… Show more

Help me understand this report

Search citation statements

Order By: Relevance

Paper Sections

Select...
2
1
1
1

Citation Types

1
4
0

Year Published

2013
2013
2021
2021

Publication Types

Select...
6

Relationship

0
6

Authors

Journals

citations
Cited by 7 publications
(5 citation statements)
references
References 45 publications
1
4
0
Order By: Relevance
“…Furthermore, chronic cigarette smoke exposure causes mitochondrial dysfunction in lung epithelial cells (Hoffmann et al , ). This is in agreement with the findings that cigarette smoke hampers exercise‐induced an increase in mitochondria density through a biogenesis response in the brain (Speck et al , ). This may be due to the reduction in PGC1α, a master regulator of mitochondrial biogenesis in the cells of COPD patients compared with cells from non‐smokers and smokers (Hoffmann et al , ).…”
Section: Mitochondrial Dysfunction In Chronic Lung Diseasessupporting
confidence: 92%
“…Furthermore, chronic cigarette smoke exposure causes mitochondrial dysfunction in lung epithelial cells (Hoffmann et al , ). This is in agreement with the findings that cigarette smoke hampers exercise‐induced an increase in mitochondria density through a biogenesis response in the brain (Speck et al , ). This may be due to the reduction in PGC1α, a master regulator of mitochondrial biogenesis in the cells of COPD patients compared with cells from non‐smokers and smokers (Hoffmann et al , ).…”
Section: Mitochondrial Dysfunction In Chronic Lung Diseasessupporting
confidence: 92%
“…Exposure to cigarettes can lead to mitochondrial dysfunction (Miro et al 1999;Anbarasi et al 2005b), as demonstrated by increased levels of cholesterol, lipid peroxides and increased cholesterol/phospholipid ratio, in conjunction with decreased mitochondrial enzymes in those exposed to cigarette smoke. However, chronic cigarette smoking was not associated with derangement of mitochondrial function in a separate study, but did prevent exercise-induced improvement in mitochondrial function (Speck et al 2011). A potential explanation for absence of demonstrable mitochondrial dysfunction in this study may relate to the use of SWISS mice in the experimental design that were demonstrated to be highly resistant to cigarette smoke-induced oxidative stress (Rueff-Barroso et al 2010).…”
Section: Mitochondrial Functionmentioning
confidence: 58%
“…However, chronic cigarette smoking was not associated with derangement of mitochondrial function in a separate study, but did prevent exercise‐induced improvement in mitochondrial function (Speck et al. ). A potential explanation for absence of demonstrable mitochondrial dysfunction in this study may relate to the use of SWISS mice in the experimental design that were demonstrated to be highly resistant to cigarette smoke‐induced oxidative stress (Rueff‐Barroso et al.…”
Section: Laboratory/biological Studiesmentioning
confidence: 99%
“…In Beas-2B lung cells treated with cigarette smoke (CS) extract, the changes in mitochondrial structure persisted for at least 3 months following 3 months of CS extract treatments (Hoffmann, Zarrintan, 2013). Similarly, tobacco smoke impairs ETC complex function in the brain and reflecting mitochondrial dysfunction systemically (Speck et al, 2011). This is also observed in muscle cells in COPD subjects where mitochondrial dysfunction may contribute to loss of strength as a systemic manifestation of COPD.…”
Section: Mitochondrial Stress Responsementioning
confidence: 99%