Reversible inhibition of mitochondrial complex IV activity in PBMC following acute smoking

Alonso, Josep R.; Cardellach, F; Casademont, Jordi; Miró, Ò

doi:10.1183/09031936.03.00038203

Cited by 46 publications

(34 citation statements)

References 39 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…A decrease in ComplexIV activity has been reported in chronic human smokers [32]. Increased oxidative stress caused by CS, especially in the lung, also induces changes in mitochondrial functions, inducing apoptosis and alterations in bioenergetics [33].…”

Section: Discussionmentioning

confidence: 99%

Short-Term Effects of Nose-Only Cigarette Smoke Exposure on Glutathione Redox Homeostasis, Cytochrome P450 1A1/2 and Respiratory Enzyme Activities in Mice Tissues

Raza¹,

John²,

Nemmar³

2013

Cell Physiol Biochem

42,540

View full text Add to dashboard Cite

Background/Aims: The components of cigarette smoke (CS) have been implicated in the development of cancer as well as in cardiopulmonary diseases. We have previously reported increased oxidative stress in rat tissues induced by tobacco-specific toxins nicotine and 4-(N-methyl-N-nitrosamino)-1-(3-pyridyl)-1-butanone (NNK). Recently, we have also shown increased oxidative stress and associated inflammatory responses in various tissues after exposure to cigarette smoke. Methods: In this study, we have further investigated the effects of nose-only cigarette smoke exposure on mitochondrial functions and glutathione-dependent redox metabolism in tissues of BALB/C mice. Liver, kidney, heart and lung tissues were analyzed for oxidative stress, glutathione (GSH) and cytochrome P450 dependent enzyme activities and mitochondrial functions after exposure to smoke generated by 9 cigarettes/day for 4 days. Control mice were exposed to air only. Results: An increase in oxidative stress as observed by increased production of reactive oxygen species (ROS) and altered GSH metabolism was apparent in all the tissues, but lung and heart appeared to be the main targets. Increased expression and activity of CYP450 1A1 and 1A2 were also observed in the tissues after exposure to cigarette smoke. Mitochondrial respiratory dysfunction in the tissues, as observed by alterations in the activities of Complex I and IV enzymes, was also observed after exposure to cigarette smoke. SDS-PAGE and Western blot results also indicate that alterations in the expression of enzyme proteins were in accordance with the changes in their catalytic functions. Conclusion: These results suggest that even short term exposure of cigarette smoke have adverse effects on mitochondrial functions and redox homeostasis in tissues which may progress to further complications associated with chronic smoking.

show abstract

Section: Discussionmentioning

confidence: 99%

Short-Term Effects of Nose-Only Cigarette Smoke Exposure on Glutathione Redox Homeostasis, Cytochrome P450 1A1/2 and Respiratory Enzyme Activities in Mice Tissues

Raza¹,

John²,

Nemmar³

2013

Cell Physiol Biochem

42,540

View full text Add to dashboard Cite

show abstract

“…The particulate and gas phases of cigarette smoke contain many toxic compounds (e.g., carbon monoxide, free radicals, nitrosamines, polynuclear aromatic compounds; Fowles et al, 2000) that may directly or indirectly compromise brain tissue. For example, carbon monoxide (CO) levels are significantly higher in smokers (Deveci et al, 2004) which is associated with lower effective hemoglobin concentrations and, consequently, diminished oxygen carrying capacity of the blood (Macdonald et al, 2004), as well as decreased efficiency of the mitochondrial respiratory chain (Alonso et al, 2004). Chronic smoking has also been equated to a type of repeated acute (mild) CO poisoning (Alonso et al, 2004), and is linked to nocturnal hypoxia (Casasola et al, 2002) as well as to respiratory risks such as chronic obstructive pulmonary disease and other conditions that may diminish or compromise lung function (Bartal, 2001).…”

Section: Potential Mechanisms For Neocortical Gm Dysmorphology In Conmentioning

confidence: 99%

Non-treatment-seeking heavy drinkers: Effects of chronic cigarette smoking on brain structure

Durazzo

Cardenas

Studholme

et al. 2007

Drug and Alcohol Dependence

View full text Add to dashboard Cite

We previously reported [Cardenas, V.A., Studholme, C., Meyerhoff, D.J., Song, E., Weiner, M.W., 2005. Chronic active heavy drinking and family history of problem drinking modulate regional brain tissue volumes. Psychiatry Res. 138, 115−130] that non-treatment-seeking, active heavy drinkers (HD) demonstrated smaller regional neocortical gray matter volumes compared to light drinking controls; however, the potential effects of chronic cigarette smoking on regional brain volumes were not addressed. The goal of this retrospective analysis was to determine if chronic smoking affected brain structure in the non-treatment-seeking heavy drinking sample from our earlier report (i.e., Cardenas et al., 2005). Regional volumetric comparisons were made among age-matched smoking HD (n = 17), non-smoking HD (n = 16), and non-smoking light drinkers (nsLD; n = 20) from our original sample. Quantitative volumetric measures of neocortical gray matter (GM), white matter (WM), subcortical structures, and cerebral spinal fluid (CSF) were derived from high-resolution magnetic resonance imaging. Smoking HD demonstrated smaller volumes than nsLD in the frontal, parietal, temporal GM, and for total neocortical GM. Smoking HD also demonstrated smaller temporal and total GM volumes than non-smoking HD. Non-smoking HD and nsLD did not differ significantly on GM volumes. Further, the three groups did not differ on lobar WM, subcortical structures or regional CSF volumes. These retrospective analyses indicate neocortical GM volume reductions in non-treatment-seeking smoking HD, but not in non-smoking HD, which are consistent with our studies in recently detoxified treatment-seeking alcohol-dependent samples.

show abstract

“…Is the residual functional impairment after successful revascularization the result of residual skeletal muscle mitochondrial dysfunction? Does smoking acutely affect walking performance in PAD due to inhibition of cytochrome oxidase 47 and furthering the degree of electron transport chain dysfunction?…”

Section: à14mentioning

confidence: 99%

Skeletal muscle metabolic changes in peripheral arterial disease contribute to exercise intolerance: a point-counterpoint discussion

2004

View full text Add to dashboard Cite

Patients with claudication have a marked impairment in exercise performance. Several factors contribute to this limitation, including reductions in large vessel blood flow and oxygen delivery as well as metabolic abnormalities in skeletal muscle. The relative contribution of these factors and their role in the pathophysiology of the exercise limitation is discussed using a point-counterpoint approach. Future directions for research conclude the discussion.

show abstract

Reversible inhibition of mitochondrial complex IV activity in PBMC following acute smoking

Cited by 46 publications

References 39 publications

Short-Term Effects of Nose-Only Cigarette Smoke Exposure on Glutathione Redox Homeostasis, Cytochrome P450 1A1/2 and Respiratory Enzyme Activities in Mice Tissues

Short-Term Effects of Nose-Only Cigarette Smoke Exposure on Glutathione Redox Homeostasis, Cytochrome P450 1A1/2 and Respiratory Enzyme Activities in Mice Tissues

Non-treatment-seeking heavy drinkers: Effects of chronic cigarette smoking on brain structure

Skeletal muscle metabolic changes in peripheral arterial disease contribute to exercise intolerance: a point-counterpoint discussion

Contact Info

Product

Resources

About