A study of reactive oxygen species in mainstream of cigarette

Huang, Mingfeng; Lin, Wan-Ting; C., Y.

doi:10.1111/j.1600-0668.2005.00330.x

Cited by 105 publications

(92 citation statements)

References 14 publications

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“…Lungs from mice exposed to cigarette smoke show increased volume fractions of alveolar septa and airspaces by morphometrical analysis and have increased MMP12 in lung macrophages compared with sham-treated mice, pathological changes consistent with those seen in human emphysema (281). These effects may be mediated by ROS, since as mentioned above, cigarette smoke contains high concentrations of ROS (110).…”

Section: Environmental Factorsmentioning

confidence: 57%

“…ROS are found in high levels in cigarette smoke and are generated by mitochondria, peroxisomes, and the plasma membranes and vacuoles of activated leukocytes (72,110). Imbalances in ROS have been implicated in a variety of lung pathologies: too little may impair host defense and too much may result in tissue damage, disease, or cell death (72).…”

Section: Endogenous Inflammatory Intermediatesmentioning

confidence: 99%

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Matrix Metalloproteinases in Lung: Multiple, Multifarious, and Multifaceted

Greenlee¹,

Werb²,

Kheradmand³

2007

Physiological Reviews

407

330

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The matrix metalloproteinases (MMPs), a family of 25 secreted and cell surface-bound neutral proteinases, process a large array of extracellular and cell surface proteins under normal and pathological conditions. MMPs play critical roles in lung organogenesis, but their expression, for the most part, is downregulated after generation of the alveoli. Our knowledge about the resurgence of the MMPs that occurs in most inflammatory diseases of the lung is rapidly expanding. Although not all members of the MMP family are found within the lung tissue, many are upregulated during the acute and chronic phases of these diseases. Furthermore, potential MMP targets in the lung include all structural proteins in the extracellular matrix (ECM), cell adhesion molecules, growth factors, cytokines, and chemokines. However, what is less known is the role of MMP proteolysis in modulating the function of these substrates in vivo. Because of their multiplicity and substantial substrate overlap, MMPs are thought to have redundant functions. However, as we explore in this review, such redundancy most likely evolved as a necessary compensatory mechanism given the critical regulatory importance of MMPs. While inhibition of MMPs has been proposed as a therapeutic option in a variety of inflammatory lung conditions, a complete understanding of the biology of these complex enzymes is needed before we can reasonably consider them as therapeutic targets.

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Section: Environmental Factorsmentioning

confidence: 57%

Section: Endogenous Inflammatory Intermediatesmentioning

confidence: 99%

Matrix Metalloproteinases in Lung: Multiple, Multifarious, and Multifaceted

Greenlee¹,

Werb²,

Kheradmand³

2007

Physiological Reviews

407

330

View full text Add to dashboard Cite

show abstract

“…Because the amount of OX/ROS changes with time as smoke matures, these data suggest that freshly produced E-Cig aerosols may be more potent than "aged" E-Cig aerosols, which has important implications for their study. Indeed, with regular cigarette smoke, different biological effects are seen with freshly produced vs. aged smoke, with aged smoke often being less biologically potent, which has previously been attributed to the decline in OX/ROS over time (74). Furthermore, because OX/ROS are highly reactive, they may also react with other components in the E-Cig aerosol, further changing its chemical composition.…”

Section: Tissue/cell Type Effectsmentioning

confidence: 99%

Will chronic e-cigarette use cause lung disease?

Rowell

Tarran

2015

American Journal of Physiology-Lung Cellular and Molecular Phys

105

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Chronic tobacco smoking is a major cause of preventable morbidity and mortality worldwide. In the lung, tobacco smoking increases the risk of lung cancer, and also causes chronic obstructive pulmonary disease (COPD), which encompasses both emphysema and chronic bronchitis. E-cigarettes (E-Cigs), or electronic nicotine delivery systems, were developed over a decade ago and are designed to deliver nicotine without combusting tobacco. Although tobacco smoking has declined since the 1950s, E-Cig usage has increased, attracting both former tobacco smokers and never smokers. E-Cig liquids (e-liquids) contain nicotine in a glycerol/propylene glycol vehicle with flavorings, which are vaporized and inhaled. To date, neither E-Cig devices, nor e-liquids, are regulated by the Food and Drug Administration (FDA). The FDA has proposed a deeming rule, which aims to initiate legislation to regulate E-Cigs, but the timeline to take effect is uncertain. Proponents of E-Cigs say that they are safe and should not be regulated. Opposition is varied, with some opponents proposing that E-Cig usage will introduce a new generation to nicotine addiction, reversing the decline seen with tobacco smoking, or that E-Cigs generally may not be safe and will trigger diseases like tobacco. In this review, we shall discuss what is known about the effects of E-Cigs on the mammalian lung and isolated lung cells in vitro. We hope that collating this data will help illustrate gaps in the knowledge of this burgeoning field, directing researchers toward answering whether or not E-Cigs are capable of causing disease.

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“…176,190,191 Mainstream cigarette smoke has been said to contain 4,000 or more constituents. [22][23][24]192 Some of these, like cadmium and lead, are directly nephrotoxic. 193,194 Other constituents like tar, carbon monoxide, nicotine, and reactive oxygen species, effect kidney damage by compromising oxygenation.…”

Section: Hypertensionmentioning

confidence: 99%

Hypoxia: The Force that Drives Chronic Kidney Disease

Colgan

Shelley

2016

Clinical Medicine & Research

128

111

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In the United States the prevalence of end-stage renal disease (ESRD) reached epidemic proportions in 2012 with over 600,000 patients being treated. The rates of ESRD among the elderly are disproportionally high. Consequently, as life expectancy increases and the baby-boom generation reaches retirement age, the already heavy burden imposed by ESRD on the US health care system is set to increase dramatically. ESRD represents the terminal stage of chronic kidney disease (CKD). A large body of evidence indicating that CKD is driven by renal tissue hypoxia has led to the development of therapeutic strategies that increase kidney oxygenation and the contention that chronic hypoxia is the final common pathway to end-stage renal failure. Numerous studies have demonstrated that one of the most potent means by which hypoxic conditions within the kidney produce CKD is by inducing a sustained inflammatory attack by infiltrating leukocytes. Indispensable to this attack is the acquisition by leukocytes of an adhesive phenotype. It was thought that this process resulted exclusively from leukocytes responding to cytokines released from ischemic renal endothelium. However, recently it has been demonstrated that leukocytes also become activated independent of the hypoxic response of endothelial cells. It was found that this endothelium-independent mechanism involves leukocytes directly sensing hypoxia and responding by transcriptional induction of the genes that encode the β2-integrin family of adhesion molecules. This induction likely maintains the long-term inflammation by which hypoxia drives the pathogenesis of CKD. Consequently, targeting these transcriptional mechanisms would appear to represent a promising new therapeutic strategy.

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A study of reactive oxygen species in mainstream of cigarette

Cited by 105 publications

References 14 publications

Matrix Metalloproteinases in Lung: Multiple, Multifarious, and Multifaceted

Matrix Metalloproteinases in Lung: Multiple, Multifarious, and Multifaceted

Will chronic e-cigarette use cause lung disease?

Hypoxia: The Force that Drives Chronic Kidney Disease

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