The tobacco‐specific nitrosamine 4‐(methylnitrosamino)‐1‐(3‐pyridyl)‐1‐butanone (NNK) induces mitochondrial and nuclear DNA damage in <i>Caenorhabditis elegans</i>

Bodhicharla, Rakesh; Ryde, Ian T.; Prasad, G.L.; Meyer, Joel N.

doi:10.1002/em.21815

Cited by 19 publications

(13 citation statements)

References 55 publications

(85 reference statements)

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“…They studied toxicity of antiretroviral drugs using mitochondrial morphology, mtDNA content, quinone reduction, and RNA expression. Work from the Meyer laboratory has also helped establish C. elegans as a model for mitochondrial toxicity (Bodhicharla et al 2014;Gonzalez-Hunt et al 2014;Rooney et al 2014). They studied the effects of lowering mtDNA levels with ethidium bromide on toxic effects of aflatoxin B1, arsenite, paraquat, rotenone, and ultraviolet radiation (Gonzalez-Hunt et al 2014).…”

Section: Toxicologymentioning

confidence: 99%

Cell Biology of the Mitochondrion

2017

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In the article by A. M. van der Bliek, M. M. Sedensky, and P. G. Morgan entitled "Cell Biology of the Mitochondrion" on page 855, the second full paragraph incorrectly attributed the development of a luciferase-expressing strain in Caenorhabditis elegans to the Meyer laboratory. The sentence beginning "Perhaps most importantly. . ." was deleted and replaced with the following sentences:"In the Glover and Pettitt laboratories, Lagido et al. (2008) developed a luciferase-expressing strain that allowed in vivo assessment of relative ATP levels in C. elegans. They later described the use of this strain for monitoring toxicant effects on mitochondrial function (McLaggan et al. 2012; Lagido et al. 2015). Members from the Meyer laboratory extended the use of this strain to allow rapid evaluation of the effects of toxicants on mitochondrial function, particularly the electron transport chain, glycolysis, and fatty acid oxidation (Luz et al. 2016b)."The following references were added to the Literature Cited section:

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Section: Toxicologymentioning

confidence: 99%

Cell Biology of the Mitochondrion

2017

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“…Many human diseases involve genomic imprinting, that is, they are epigenetic. Because metals in the biosphere have profound epigenetic impacts on neurologic and other diseases it is likely that MPV17-NNH may, in addition to the demonstrated genetic factors, also depend in part on the abundance of toxic metals absorbed by such patients from the biosphere [17] .…”

Section: Discussionmentioning

confidence: 99%

MPV17-related hepatocerebral mitochondrial DNA depletion syndrome (MPV17-NNH) revisited

et al. 2016

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MPV17-related hepatocerebral mitochondrial DNA depletion syndrome (previously known as Navajo neurohepatopathy) was discovered in children in the Four Corner's region of New Mexico approximately 40 years ago. This disease is associated with a single missense mutation in exon 2 in the MPV17 gene. The syndrome has now been recognized world-wide. We find that huge quantities of neurotoxins were present in archived nervous tissues from such patients.Arsenic was increased 18 ×, cadmium ~ 10 ×, cobalt 2.5 × and manganese 2.3 ×; the largest increase was in mercury content 16,000 × compared to contemporaneous fresh-frozen normal nervous tissues.In the Four Corner's region of NM the life span is reduced compared to other parts of the United States and in our patients with MPV17-NNH the average life span was 5.4 years ± 2.7 (SE) years.We now live in the Anthropocene an epoch characterized by large additions to the biosphere of neurotoxins. The effects of such toxic loads on human health and disease remain to be assessed.We speculate how such high neurotoxin content in tissues, which is likely to increase during the Anthropocene, may have influenced MPV17-NNH and similar phenotypes in different parts of the world.Our results imply that selenium supplementation to the diet in the Four Corner's region of NM might be beneficial to normal people and in the management of patients with MPV17-NNH syndrome.

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“…Furthermore, this has been associated with the accumulation of mitochondrial DNA adducts resulting from tobacco-related carcinogen metabolism over time, as a result of insufficient repair processes in rats [84,85]. Certainly, DNA adducts formed as a result of tobacco-specific nitrosamine 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone metabolism induced both nuclear and mitochondrial DNA damage in exposed Caenorhabditis elegans, which was associated with reduced ATP production and oxygen consumption [86]. At present, investigations in the context of mouse models of human lung cancer are limited, but may provide a critical understanding of the underlying mechanisms of lung tumorigenesis.…”

Section: Mitochondrial Dysfunction In Lung Cancermentioning

confidence: 99%

Is mitochondrial dysfunction a driving mechanism linking COPD to nonsmall cell lung carcinoma?

et al. 2017

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Chronic obstructive pulmonary disease (COPD) patients are at increased risk of developing nonsmall cell lung carcinoma, irrespective of their smoking history. Although the mechanisms behind this observation are not clear, established drivers of carcinogenesis in COPD include oxidative stress and sustained chronic inflammation. Mitochondria are critical in these two processes and recent evidence links increased oxidative stress in COPD patients to mitochondrial damage. We therefore postulate that mitochondrial damage in COPD patients leads to increased oxidative stress and chronic inflammation, thereby increasing the risk of carcinogenesis.The functional state of the mitochondrion is dependent on the balance between its biogenesis and degradation (mitophagy). Dysfunctional mitochondria are a source of oxidative stress and inflammasome activation. In COPD, there is impaired translocation of the ubiquitin-related degradation molecule Parkin following activation of the Pink1 mitophagy pathway, resulting in excessive dysfunctional mitochondria. We hypothesise that deranged pathways in mitochondrial biogenesis and mitophagy in COPD can account for the increased risk in carcinogenesis. To test this hypothesis, animal models exposed to cigarette smoke and developing emphysema and lung cancer should be developed. In the future, the use of mitochondriabased antioxidants should be studied as an adjunct with the aim of reducing the risk of COPD-associated cancer.

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The tobacco‐specific nitrosamine 4‐(methylnitrosamino)‐1‐(3‐pyridyl)‐1‐butanone (NNK) induces mitochondrial and nuclear DNA damage in Caenorhabditis elegans

Cited by 19 publications

References 55 publications

Cell Biology of the Mitochondrion

Cell Biology of the Mitochondrion

MPV17-related hepatocerebral mitochondrial DNA depletion syndrome (MPV17-NNH) revisited

Is mitochondrial dysfunction a driving mechanism linking COPD to nonsmall cell lung carcinoma?

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