Mitochondrial toxicity of tobacco smoke and air pollution

Fetterman, Jessica L.; Sammy, Melissa J; Ballinger, Scott W.

doi:10.1016/j.tox.2017.08.002

Cited by 81 publications

(48 citation statements)

References 306 publications

(368 reference statements)

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“…Tobaco smoke (TBS) emits a wide range of gases, aerosolized liquids, and fine particulate matter including VOC and formaldehyde, nitrogen oxide, PM2.5, and nicotine. 50 , 51 TBS is estimated to cause approximately 480,000 excess deaths per year, 52 and it can contribute to 30% of all cancer deaths. 53 Among other actions, TBS can induce DNA damage, 51 change in sputum (mucin) quality, and depressed antioxidant and antimicrobial activity in smokers and among COPD patients.…”

Section: Characteristics Of Air Pollutantsmentioning

confidence: 99%

“… 50 , 51 TBS is estimated to cause approximately 480,000 excess deaths per year, 52 and it can contribute to 30% of all cancer deaths. 53 Among other actions, TBS can induce DNA damage, 51 change in sputum (mucin) quality, and depressed antioxidant and antimicrobial activity in smokers and among COPD patients. 54 , 55 …”

Section: Characteristics Of Air Pollutantsmentioning

confidence: 99%

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Immunopathological features of air pollution and its impact on inflammatory airway diseases (IAD)

Rouadi¹,

Idriss²,

Naclerio³

et al. 2020

World Allergy Organization Journal

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Air pollution causes significant morbidity and mortality in patients with inflammatory airway diseases (IAD) such as allergic rhinitis (AR), chronic rhinosinusitis (CRS), asthma, and chronic obstructive pulmonary disease (COPD). Oxidative stress in patients with IAD can induce eosinophilic inflammation in the airways, augment atopic allergic sensitization, and increase susceptibility to infection. We reviewed emerging data depicting the involvement of oxidative stress in IAD patients. We evaluated biomarkers, outcome measures and immunopathological alterations across the airway mucosal barrier following exposure, particularly when accentuated by an infectious insult.

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Section: Characteristics Of Air Pollutantsmentioning

confidence: 99%

Section: Characteristics Of Air Pollutantsmentioning

confidence: 99%

Immunopathological features of air pollution and its impact on inflammatory airway diseases (IAD)

Rouadi¹,

Idriss²,

Naclerio³

et al. 2020

World Allergy Organization Journal

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“…Airborne pollution and cigarette smoke can cause various diseases including birth defects, cardiovascular diseases, respiratory diseases, neurological disorders, and cancer (Stingone et al, 2014;Fetterman et al, 2017;Boovarahan and Kurian, 2018). Airborne particulate matter (PM) can be classified into three categories based on their size: coarse (PM 10 < 10 μm diameter), fine (PM 2.5 < 10 μm diameter), and ultrafine or nano (PM 0.2 < 0.2 μm).…”

Section: Impact Of Xenobiotics On Mtdna Methylationmentioning

confidence: 99%

Mitochondrial DNA: Epigenetics and environment

Sharma

Pasala

Prakash

2019

Environ and Mol Mutagen

128

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Maintenance of the mitochondrial genome is essential for proper cellular function. For this purpose, mitochondrial DNA (mtDNA) needs to be faithfully replicated, transcribed, translated, and repaired in the face of constant onslaught from endogenous and environmental agents. Although only 13 polypeptides are encoded within mtDNA, the mitochondrial proteome comprises over 1500 proteins that are encoded by nuclear genes and translocated to the mitochondria for the purpose of maintaining mitochondrial function. Regulation of mtDNA and mitochondrial proteins by epigenetic changes and post‐translational modifications facilitate crosstalk between the nucleus and the mitochondria and ultimately lead to the maintenance of cellular health and homeostasis. DNA methyl transferases have been identified in the mitochondria implicating that methylation occurs within this organelle; however, the extent to which mtDNA is methylated has been debated for many years. Mechanisms of demethylation within this organelle have also been postulated, but the exact mechanisms and their outcomes is still an active area of research. Mitochondrial dysfunction in the form of altered gene expression and ATP production, resulting from epigenetic changes, can lead to various conditions including aging‐related neurodegenerative disorders, altered metabolism, changes in circadian rhythm, and cancer. Here, we provide an overview of the epigenetic regulation of mtDNA via methylation, long and short noncoding RNAs, and post‐translational modifications of nucleoid proteins (as mitochondria lack histones). We also highlight the influence of xenobiotics such as airborne environmental pollutants, contamination from heavy metals, and therapeutic drugs on mtDNA methylation. Environ. Mol. Mutagen., 60:668–682, 2019. © 2019 Wiley Periodicals, Inc.

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“…39,40 Cigarette smoking also induces insulin resistance, which may lead to hyperinsulinaemia, as observed by a marked decrease in lipoprotein lipase and hepatic lipase that transforms VLDL to LDL. 41 Insulin resistance was shown to negatively affect the lipid profile, inducing endothelial dysfunction and oxidative stress and driving the formation of atheroma and the development of cardiovascular diseases. 40 In our study, moderate to strong positive correlations were found between both total cholesterol and triglycerides and O 2 As a rich source of active oxidants, cigarette smoke may cause an imbalance in the endogenous antioxidant defences that are associated with increased production of free ROS.…”

Section: Discussionmentioning

confidence: 99%

Comparative assessment of individual RONS in serum of smokers compared with non-smokers and their correlation with the lipid profile and antioxidant status

Khojah

Ahmed

2019

J Int Med Res

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Objective Cigarette smoking generates free radicals, such as reactive oxygen and nitrogen species (RONS) that contribute to many diseases. The aim of this study was to compare the levels of individual RONS in serum from smokers and non-smokers, and to examine their impact on lipid profiles and the endogenous antioxidant status, which is represented by vitamins C and E. Methods Ninety-four healthy Egyptian volunteers (48 smokers and 46 non-smokers) were enrolled. Blood samples were collected and analysed for common haematological tests, lipid profiles, and serum antioxidants. Six reactive oxygen species and three reactive nitrogen species were measured. Results A significant increase in radical levels was observed, as well as significant increases in haemoglobin (Hb), haematocrit, platelet count, total cholesterol, triglycerides, low-density lipoprotein cholesterol, and very low-density lipoprotein cholesterol in smokers compared with non-smokers. In contrast, high-density lipoprotein cholesterol was significantly reduced in smokers compared with non-smokers. A moderate negative correlation was found between serum levels of vitamins C and E and O2–•, HO•, H2O2, NO•, and ONO•, reflecting a negative impact of elevated RONS levels on the endogenous antioxidant status. Conclusion These results may increase our understanding of the pathological role of smoking in several diseases.

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Mitochondrial toxicity of tobacco smoke and air pollution

Cited by 81 publications

References 306 publications

Immunopathological features of air pollution and its impact on inflammatory airway diseases (IAD)

Immunopathological features of air pollution and its impact on inflammatory airway diseases (IAD)

Mitochondrial DNA: Epigenetics and environment

Comparative assessment of individual RONS in serum of smokers compared with non-smokers and their correlation with the lipid profile and antioxidant status

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