Tobacco nitrosamines as culprits in disease: mechanisms reviewed

Yalçın, Emine; Monte, Suzanne M. de la

doi:10.1007/s13105-016-0465-9

Cited by 58 publications

(49 citation statements)

References 87 publications

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“…Smoking is yet another avoidable risk factor for AD neurodegeneration as it increases neuro-inflammation, tau phosphorylation and Aβ42 deposition [150]. Other potential exposure-mediated causes of neurodegeneration linked to insulin resistance include neurotoxins [151], particulate matter present in polluted air [152, 153], and nitrosamines incorporated into processed and preserved foods and tobacco [154–158]. …”

Section: Therapeutic Strategies For Abrogating Brain Insulin Deficimentioning

confidence: 99%

Insulin Resistance and Neurodegeneration: Progress Towards the Development of New Therapeutics for Alzheimer’s Disease

Monte

2016

Drugs

214

140

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Alzheimer’s disease (AD) should be regarded as a degenerative metabolic disease caused by brain insulin resistance and deficiency, and overlapping with the molecular, biochemical, pathophysiological, and metabolic dysfunctions occurring in diabetes mellitus, non-alcoholic fatty liver disease, and metabolic syndrome. Although most of the diagnostic and therapeutic approaches over the past several decades have focused on amyloid-beta (Aβ42) and aberrantly phosphorylated tau, which could be caused by consequences of brain insulin resistance, the broader array of pathologies including white matter atrophy with loss of myelinated fibrils and leukoaraiosis, non-Aβ42 microvascular disease, dysregulated lipid metabolism, mitochondrial dysfunction, astrocytic gliosis, neuro-inflammation, and loss of synapses vis-à-vis growth of dystrophic neurites, is not readily accounted for by Aβ42 accumulations, but could be explained by dysregulated insulin/IGF-1 signaling with attendant impairments in signal transduction and gene expression. This review covers the diverse range of brain abnormalities in AD and discusses how insulins, incretins, and insulin sensitizers could be utilized to treat at different stages of neurodegeneration.

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Section: Therapeutic Strategies For Abrogating Brain Insulin Deficimentioning

confidence: 99%

Insulin Resistance and Neurodegeneration: Progress Towards the Development of New Therapeutics for Alzheimer’s Disease

Monte

2016

Drugs

214

140

View full text Add to dashboard Cite

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“…Combustion derived products, including CS, are well known for their pro-inflammatory effects which alter the endothelium and lead to endothelial dysfunction [189][190][191]. Lind et al…”

Section: Forearm Blood Flowmentioning

confidence: 99%

Electronic cigarettes increase endothelial progenitor cells in the blood of healthy volunteers

et al. 2016

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“…For example, NNK induces oxidative stress which causes DNA damage, such as adductions and mutations, via increased levels of intracellular reactive oxygen species (ROS) and result in lung cancer progression (Yalcin and de la Monte, 2016). NNK also induces Akt-dependent proliferation and NFκB-dependent survival of nonsmall cell lung carcinoma cells (Tsurutani et al, 2005).…”

Section: Introductionmentioning

confidence: 99%

Tobacco nitrosamine NNK increases ALDH-positive cells via ROS-Wnt signaling pathway in A549 human lung cancer cells

et al. 2017

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-Epidemiological studies suggest that lung cancer, which is a major cause of cancer death, has a critical association with cigarette smoking. Tobacco-specific nitrosamine 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK) in cigarette smoke is a major risk factor for carcinogenesis. However, the mechanisms by which NNK promotes cancer development have not been fully elucidated. Growing evidence suggests that lung cancer originates from cancer stem cells (CSCs), which are a minor population of lung cancer cells. In the present study, we investigated the effects of NNK on the CSCs in A549 human lung cancer cells using flow cytometry with aldehyde dehydrogenase (ALDH), a functional marker of CSCs. We found that NNK increased the proportion of ALDH-positive cells in a dose-dependent manner. A Wnt inhibitor PNU74654 reduced NNK-induced expression levels of Wnt target gene Dkk1 and increase in ALDH-positive cells. We next examined the signaling pathway that mediates the NNKinduced increase in ALDH-positive cells via Wnt signaling. DCF assay revealed that NNK induced reactive oxygen species (ROS) production. The ROS scavenger N-acetylcysteine (NAC) inhibited the NNKinduced Wnt activation and increase in ALDH-positive cells. These data suggest that NNK-induced ROS activate the Wnt signaling pathway in A549 cells. These findings would provide new insights into the role of NNK in the lung CSCs.

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Tobacco nitrosamines as culprits in disease: mechanisms reviewed

Cited by 58 publications

References 87 publications

Insulin Resistance and Neurodegeneration: Progress Towards the Development of New Therapeutics for Alzheimer’s Disease

Insulin Resistance and Neurodegeneration: Progress Towards the Development of New Therapeutics for Alzheimer’s Disease

Electronic cigarettes increase endothelial progenitor cells in the blood of healthy volunteers

Tobacco nitrosamine NNK increases ALDH-positive cells via ROS-Wnt signaling pathway in A549 human lung cancer cells

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