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  1. Article ; Online: Comprehensive review of epidemiological and animal studies on the potential carcinogenic effects of nicotine per se.

    Haussmann, Hans-Juergen / Fariss, Marc W

    Critical reviews in toxicology

    2016  Volume 46, Issue 8, Page(s) 701–734

    Abstract: The effects of long-term use of nicotine per se on cancer risk, in the absence of tobacco extract or smoke, are not clearly understood. This review evaluates the strength of published scientific evidence, in both epidemiological and animal studies, for ... ...

    Abstract The effects of long-term use of nicotine per se on cancer risk, in the absence of tobacco extract or smoke, are not clearly understood. This review evaluates the strength of published scientific evidence, in both epidemiological and animal studies, for the potential carcinogenic effects of nicotine per se; that is to act as a complete carcinogen or as a modulator of carcinogenesis. For human studies, there appears to be inadequate evidence for an association between nicotine exposure and the presence of or lack of a carcinogenic effect due to the limited information available. In animal studies, limited evidence suggests an association between long-term nicotine exposure and a lack of a complete carcinogenic effect. Conclusive studies using current bioassay guidelines, however, are missing. In studies using chemical/physical carcinogens or transgenic models, there appears to be inadequate evidence for an association between nicotine exposure and the presence of or lack of a modulating (stimulating) effect on carcinogenesis. This is primarily due to the large number of conflicting studies. In contrast, a majority of studies provides sufficient evidence for an association between nicotine exposure and enhanced carcinogenesis of cancer cells inoculated in mice. This modulating effect was especially prominent in immunocompromized mice. Overall, taking the human and animal studies into consideration, there appears to be inadequate evidence to conclude that nicotine per se does or does not cause or modulate carcinogenesis in humans. This conclusion is in agreement with the recent US Surgeon General's 2014 report on the health consequences of nicotine exposure.
    MeSH term(s) Animals ; Carcinogens/toxicity ; Epidemiologic Measurements ; Humans ; Models, Animal ; Nicotine/toxicity
    Chemical Substances Carcinogens ; Nicotine (6M3C89ZY6R)
    Language English
    Publishing date 2016-06-09
    Publishing country England
    Document type Journal Article ; Review
    ZDB-ID 1097071-x
    ISSN 1547-6898 ; 1040-8444
    ISSN (online) 1547-6898
    ISSN 1040-8444
    DOI 10.1080/10408444.2016.1182116
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  2. Article ; Online: A systematic review of possible serious adverse health effects of nicotine replacement therapy.

    Lee, Peter N / Fariss, Marc W

    Archives of toxicology

    2016  Volume 91, Issue 4, Page(s) 1565–1594

    Abstract: We conducted a systematic literature review to identify and critically evaluate studies of serious adverse health effects (SAHEs) in humans using nicotine replacement therapy (NRT) products. Serious adverse health effects refer to adverse events, leading ...

    Abstract We conducted a systematic literature review to identify and critically evaluate studies of serious adverse health effects (SAHEs) in humans using nicotine replacement therapy (NRT) products. Serious adverse health effects refer to adverse events, leading to substantial disruption of the ability to conduct normal life functions. Strength of evidence evaluations and conclusions were also determined for the identified SAHEs. We evaluated 34 epidemiological studies and clinical trials, relating NRT use to cancer, reproduction/development, CVD, stroke and/or other SAHEs in patients, and four meta-analyses on effects in healthy populations. The overall evidence suffers from many limitations, the most significant being the short-term exposure (≤12 weeks) and follow-up to NRT product use in most of the studies, the common failure to account for changes in smoking behaviour following NRT use, and the sparse information on SAHEs by type of NRT product used. The only SAHE from NRT exposure we identified was an increase in respiratory congenital abnormalities reported in one study. Limited evidence indicated a lack of effect between NRT exposure and SAHEs for CVD and various reproduction/developmental endpoints. For cancer, stroke and other SAHEs, the evidence was inadequate to demonstrate any association with NRT use. Our conclusions agree with recent statements from authoritative bodies.
    MeSH term(s) Humans ; Smoking Cessation/methods ; Smoking Prevention ; Time Factors ; Tobacco Use Cessation Devices/adverse effects
    Language English
    Publishing date 2016-10-03
    Publishing country Germany
    Document type Journal Article ; Review ; Systematic Review
    ZDB-ID 124992-7
    ISSN 1432-0738 ; 0340-5761
    ISSN (online) 1432-0738
    ISSN 0340-5761
    DOI 10.1007/s00204-016-1856-y
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  3. Article ; Online: Chemical, physical, and in vitro characterization of research cigarettes containing denicotinized tobacco.

    Coffa, Bonnie G / Coggins, Christopher R E / Werley, Michael S / Oldham, Michael J / Fariss, Marc W

    Regulatory toxicology and pharmacology : RTP

    2016  Volume 79, Page(s) 64–73

    Abstract: The use of very low nicotine tobacco cigarettes is currently being investigated as a possible harm reduction strategy. Here, we report the smoke chemistry, toxicity, and physical characteristics of very low nicotine cigarettes that were made using ... ...

    Abstract The use of very low nicotine tobacco cigarettes is currently being investigated as a possible harm reduction strategy. Here, we report the smoke chemistry, toxicity, and physical characteristics of very low nicotine cigarettes that were made using blended tobacco processed through a supercritical CO2 fluid extraction, which resulted in elimination of 96% of nicotine content (denicotinized (denic) tobacco). Three types of test cigarettes (TCs) were manufactured with tobacco filler containing 100% denic tobacco (TC100), 50% denic tobacco and 50% unextracted tobacco (TC50/50), and 100% unextracted tobacco (TC0). Mainstream smoke (MS) was generated for measurement of 46 analytes and cytotoxicity and mutagenicity determination. Analysis of physical characteristics of TCs demonstrated they were well made with <5% variability among cigarettes for most parameters measured. We observed significant changes in the levels of smoke constituents, including decreases in formaldehyde, nitrosamines, and phenol, and increases in aliphatic hydrocarbons, aliphatic nitrogen compounds, aromatic amines, halogen compounds, and metals. Use of denic tobacco resulted in changes in the chemical composition of MS, but these changes did not modify biological activity as measured in the mutagenicity and cytotoxicity assays.
    MeSH term(s) 3T3 Cells ; Animals ; Chromatography, Supercritical Fluid ; Consumer Product Safety ; DNA, Bacterial/drug effects ; DNA, Bacterial/genetics ; Fibroblasts/drug effects ; Fibroblasts/pathology ; Humans ; Mice ; Mutagenesis ; Mutagenicity Tests ; Mutation ; Nicotine/analysis ; Nicotine/toxicity ; Nicotinic Agonists/analysis ; Nicotinic Agonists/toxicity ; Risk Assessment ; Salmonella typhimurium/drug effects ; Salmonella typhimurium/genetics ; Smoke/adverse effects ; Smoke/analysis ; Smoking/adverse effects ; Nicotiana/chemistry ; Nicotiana/toxicity ; Tobacco Products/analysis ; Tobacco Products/toxicity
    Chemical Substances DNA, Bacterial ; Nicotinic Agonists ; Smoke ; Nicotine (6M3C89ZY6R)
    Language English
    Publishing date 2016-05-13
    Publishing country Netherlands
    Document type Comparative Study ; Journal Article
    ZDB-ID 604672-1
    ISSN 1096-0295 ; 0273-2300
    ISSN (online) 1096-0295
    ISSN 0273-2300
    DOI 10.1016/j.yrtph.2016.05.016
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  4. Article ; Online: Fluorescence microplate reader measurement of tissue susceptibility to lipid peroxidation.

    Zhang, Jin-Gang / Fariss, Marc W

    Current protocols in toxicology

    2004  Volume Chapter 17, Page(s) Unit17.3

    Abstract: This unit describes a method for the measurement of cellular membrane antioxidant capacity or susceptibility of tissue samples to lipid peroxidation using a fluorescence microplate reader. The assay is simple and has the advantage of monitoring ... ...

    Abstract This unit describes a method for the measurement of cellular membrane antioxidant capacity or susceptibility of tissue samples to lipid peroxidation using a fluorescence microplate reader. The assay is simple and has the advantage of monitoring susceptibility to lipid peroxidation in a large number of samples in real time.
    MeSH term(s) Animals ; Antioxidants/metabolism ; Cell Membrane/metabolism ; Lipid Peroxidation ; Spectrometry, Fluorescence/instrumentation ; Spectrometry, Fluorescence/methods
    Chemical Substances Antioxidants
    Language English
    Publishing date 2004-02
    Publishing country United States
    Document type Journal Article
    ISSN 1934-9262
    ISSN (online) 1934-9262
    DOI 10.1002/0471140856.tx1703s18
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  5. Article ; Online: Emerging mechanistic targets in lung injury induced by combustion-generated particles.

    Fariss, Marc W / Gilmour, M Ian / Reilly, Christopher A / Liedtke, Wolfgang / Ghio, Andrew J

    Toxicological sciences : an official journal of the Society of Toxicology

    2013  Volume 132, Issue 2, Page(s) 253–267

    Abstract: The mechanism for biological effect following exposure to combustion-generated particles is incompletely defined. The identification of pathways regulating the acute toxicological effects of these particles provides specific targets for therapeutic ... ...

    Abstract The mechanism for biological effect following exposure to combustion-generated particles is incompletely defined. The identification of pathways regulating the acute toxicological effects of these particles provides specific targets for therapeutic manipulation in an attempt to impact disease following exposures. Transient receptor potential (TRP) cation channels were identified as "particle sensors" in that their activation was coupled with the initiation of protective responses limiting airway deposition and inflammatory responses, which promote degradation and clearance of the particles. TRPA1, V1, V4, and M8 have a capacity to mediate adverse effects after exposure to combustion-generated particulate matter (PM); relative contributions of each depend upon particle composition, dose, and deposition. Exposure of human bronchial epithelial cells to an organic extract of diesel exhaust particle was followed by TRPV4 mediating Ca(++) influx, increased RAS expression, mitogen-activated protein kinase signaling, and matrix metalloproteinase-1 activation. These novel pathways of biological effect can be targeted by compounds that specifically inhibit critical signaling reactions. In addition to TRPs and calcium biochemistry, humic-like substances (HLS) and cell/tissue iron equilibrium were identified as potential mechanistic targets in lung injury after particle exposure. In respiratory epithelial cells, iron sequestration by HLS in wood smoke particle (WSP) was associated with oxidant generation, cell signaling, transcription factor activation, and release of inflammatory mediators. Similar to WSP, cytotoxic insoluble nanosized spherical particles composed of HLS were isolated from cigarette smoke condensate. Therapies that promote bioelimination of HLS and prevent the disruption of iron homeostasis could function to reduce the harmful effects of combustion-generated PM exposure.
    MeSH term(s) Air Pollutants/toxicity ; Calcium/metabolism ; Cells, Cultured ; Humans ; Iron/metabolism ; Lung/drug effects ; Lung/metabolism ; Microscopy, Electron, Scanning ; Microscopy, Electron, Transmission ; Mitochondria/metabolism ; Particle Size ; Smoke ; Nicotiana ; Transient Receptor Potential Channels/metabolism
    Chemical Substances Air Pollutants ; Smoke ; Transient Receptor Potential Channels ; Iron (E1UOL152H7) ; Calcium (SY7Q814VUP)
    Language English
    Publishing date 2013-01-14
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 1420885-4
    ISSN 1096-0929 ; 1096-6080
    ISSN (online) 1096-0929
    ISSN 1096-6080
    DOI 10.1093/toxsci/kft001
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    Zs.A 1709: Show issues Location:
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  6. Article: Vitamin E therapy in Parkinson's disease.

    Fariss, Marc W / Zhang, Jin-Gang

    Toxicology

    2003  Volume 189, Issue 1-2, Page(s) 129–146

    Abstract: Though the etiology is not well understood, late-onset Parkinson's disease (PD) appears to result from several key factors including exposure to unknown environmental toxicants, toxic endogenous compounds and genetic alterations. A plethora of scientific ...

    Abstract Though the etiology is not well understood, late-onset Parkinson's disease (PD) appears to result from several key factors including exposure to unknown environmental toxicants, toxic endogenous compounds and genetic alterations. A plethora of scientific evidence suggest that these environmental and endogenous factors cause PD by producing mitochondrial (mito) oxidative stress and damage in the substantia nigra, leading to cell death. Thus assuming a critical role for mito oxidative stress in PD, therapies to treat or prevent PD must target these mito and protect them against oxidative damage. The focus of this article is to briefly review the experimental and clinical evidence for the role of environmental toxicants and mito oxidative stress/damage in PD as well as discuss the potential protective role of mito d-alpha-tocopherol (T) enrichment and vitamin E therapy in PD. New experimental data are presented that supports the enrichment of mito with T as a critical event in cytoprotection against toxic mito-derived oxidative stress. We propose that chronic, high dose vitamin E dietary supplementation or parenteral vitamin E administration (e.g. vitamin E succinate) may serve as a successful therapeutic strategy for the prevention or treatment of PD (by enriching substantia nigra mito with protective levels of T).
    MeSH term(s) Animals ; Antioxidants/metabolism ; Antioxidants/therapeutic use ; Dietary Supplements ; Humans ; Mitochondria/metabolism ; Oxidative Stress/drug effects ; Oxidative Stress/physiology ; Parkinson Disease/drug therapy ; Parkinson Disease/etiology ; Parkinson Disease/metabolism ; alpha-Tocopherol/metabolism ; alpha-Tocopherol/therapeutic use
    Chemical Substances Antioxidants ; alpha-Tocopherol (H4N855PNZ1)
    Language English
    Publishing date 2003-07-15
    Publishing country Ireland
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, P.H.S. ; Review
    ZDB-ID 184557-3
    ISSN 1879-3185 ; 0300-483X
    ISSN (online) 1879-3185
    ISSN 0300-483X
    DOI 10.1016/s0300-483x(03)00158-6
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  7. Article ; Online: Role of plasma membrane disruption in reference moist smokeless tobacco-induced cell death.

    Joyce, Andrew R / Hawkins, William / Fariss, Marc W / Sengupta, Tapas K

    Toxicology letters

    2010  Volume 198, Issue 2, Page(s) 191–199

    Abstract: An oral injury is thought to presage the development of mucosal lesions that are common in moist smokeless tobacco (MST) users. The abrasion or mechanical stress caused by direct contact of MST with the oral mucosa may contribute to this injury by ... ...

    Abstract An oral injury is thought to presage the development of mucosal lesions that are common in moist smokeless tobacco (MST) users. The abrasion or mechanical stress caused by direct contact of MST with the oral mucosa may contribute to this injury by causing transient disruptions in the cell membrane. In order to test this hypothesis, we developed an in vitro exposure system that directly exposes cells to reference MST on a rocking platform to simulate the abrasion that might be experienced in the oral cavity when using MST. Using this treatment paradigm, we monitored plasma membrane disruption as a measure of cell wounding caused by direct interaction of the tobacco material itself with monolayer cultures of Het-1A immortalized human esophageal cells as a potential contributor to the injury process. We found that a washed reference MST preparation, in which MST-associated chemicals were removed but the tobacco material retained, causes cell wounding as indicated by the uptake through plasma membrane disruptions of a fluorescent marker normally impermeable to the cell. Having established that non-chemical properties of MST cause cell wounding, subsequent experiments revealed that cell wounding during simultaneous exposure to an aqueous MST-extract result in greater than additive cell death when compared to treatment with washed MST or MST-extract alone. Furthermore, we found that the high levels of free calcium found in MST-extract appear to be playing an important role. Taken together, these results indicate that MST-induced oral injury may result from a combined interaction of physical disruption of the plasma membrane by the tobacco material itself and the adverse effects of MST chemical constituents, notably high levels of calcium, that gain entry to the cell by way of MST-induced cell wounding.
    MeSH term(s) Calcium/pharmacology ; Cell Culture Techniques ; Cell Death/drug effects ; Cell Line ; Cell Membrane/drug effects ; Culture Media ; Humans ; Microscopy, Fluorescence ; Models, Biological ; Mouth Mucosa/drug effects ; Mouth Mucosa/pathology ; Tobacco, Smokeless/toxicity
    Chemical Substances Culture Media ; Calcium (SY7Q814VUP)
    Language English
    Publishing date 2010-10-05
    Publishing country Netherlands
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 433788-8
    ISSN 1879-3169 ; 0378-4274
    ISSN (online) 1879-3169
    ISSN 0378-4274
    DOI 10.1016/j.toxlet.2010.06.014
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  8. Article: Thenoyltrifluoroacetone, a potent inhibitor of carboxylesterase activity.

    Zhang, Jin Gang / Fariss, Marc W

    Biochemical pharmacology

    2002  Volume 63, Issue 4, Page(s) 751–754

    Abstract: Thenoyltrifluoroacetone (TTFA), a conventional mitochondrial complex II inhibitor, was found to inhibit purified porcine liver carboxylesterase non-competitively with a K(i) of 0.61x10(-6)M and an IC(50) of 0.54x10(-6)M. Both rat plasma and liver ... ...

    Abstract Thenoyltrifluoroacetone (TTFA), a conventional mitochondrial complex II inhibitor, was found to inhibit purified porcine liver carboxylesterase non-competitively with a K(i) of 0.61x10(-6)M and an IC(50) of 0.54x10(-6)M. Both rat plasma and liver mitochondrial esterases were inhibited in a concentration-dependent fashion. Results indicate that TTFA is a potent inhibitor of carboxylesterase activity, in addition to its ability to inhibit mitochondrial complex II activity. Therefore, caution is warranted in using TTFA as a mitochondrial complex inhibitor in combination with esterase substrates, such as fluorescence probes or vitamin E esters.
    MeSH term(s) Animals ; Carboxylesterase ; Carboxylic Ester Hydrolases/antagonists & inhibitors ; Carboxylic Ester Hydrolases/blood ; Carboxylic Ester Hydrolases/isolation & purification ; Carboxylic Ester Hydrolases/metabolism ; Chelating Agents/pharmacology ; Electron Transport Complex II ; Kinetics ; Male ; Mitochondria, Liver/drug effects ; Mitochondria, Liver/enzymology ; Multienzyme Complexes/metabolism ; Oxidoreductases/metabolism ; Rats ; Rats, Sprague-Dawley ; Succinate Dehydrogenase/metabolism ; Thenoyltrifluoroacetone/pharmacology
    Chemical Substances Chelating Agents ; Multienzyme Complexes ; Thenoyltrifluoroacetone (326-91-0) ; Oxidoreductases (EC 1.-) ; Electron Transport Complex II (EC 1.3.5.1) ; Succinate Dehydrogenase (EC 1.3.99.1) ; Carboxylic Ester Hydrolases (EC 3.1.1.-) ; Carboxylesterase (EC 3.1.1.1)
    Language English
    Publishing date 2002-02-15
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, P.H.S.
    ZDB-ID 208787-x
    ISSN 1873-2968 ; 0006-2952
    ISSN (online) 1873-2968
    ISSN 0006-2952
    DOI 10.1016/s0006-2952(01)00871-1
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  9. Article ; Online: Reference moist smokeless tobacco-induced apoptosis in human monocytes/macrophages cell line MM6.

    Lombard, Catherine / Farthing, Don / Sun, Jingping / Fariss, Marc W / McKallip, Robert J

    International immunopharmacology

    2010  Volume 10, Issue 9, Page(s) 1029–1040

    Abstract: Moist smokeless tobacco use is associated with various types of oral injury, including leukoplakia and dipper's pouch, although the mechanism by which the injury is caused still remains unclear. One possible mechanism is that moist smokeless tobacco ... ...

    Abstract Moist smokeless tobacco use is associated with various types of oral injury, including leukoplakia and dipper's pouch, although the mechanism by which the injury is caused still remains unclear. One possible mechanism is that moist smokeless tobacco affects the inflammatory response. For example, a study by Johnson et al. demonstrated a reduction in the volume density of macrophages and increased inflammation and redness at the smokeless tobacco placement site when compared to non-placement site. The current study investigated the direct effect of reference moist smokeless tobacco extract (STE) exposure on the viability of MM6 monocyte/macrophage cell line. The exposure of MM6 cells to various concentrations of STE, led to a significant and dose-related decrease in cell viability. Furthermore, STE exposure resulted in an increase in Annexin V/PI positive cells, an increase in TUNEL-positive cells, and cleaved PARP staining all of which were inhibited by pre-incubation with a pan-caspase inhibitor, suggesting that the observed STE toxicity was due to the induction of apoptosis. Next, the role of various moist smokeless tobacco-derived components in STE-induced apoptosis of MM6 cells was investigated. Our findings suggest that STE-induced osmotic stress, but not exposure to nicotine, plays an important role in STE-induced apoptosis of MM6 cells. Together, these data show for the first time that STE exposure leads to the induction of apoptosis in human monocyte/macrophage cells, which appears to be induced in part, by reference STE-mediated osmotic stress.
    MeSH term(s) Annexin A5/analysis ; Apoptosis ; Caspase Inhibitors ; Cell Line ; Humans ; Leukoplakia/chemically induced ; Macrophages/drug effects ; Nicotine/toxicity ; Osmosis/physiology ; Plant Extracts/toxicity ; Tobacco, Smokeless/toxicity
    Chemical Substances Annexin A5 ; Caspase Inhibitors ; Plant Extracts ; Nicotine (6M3C89ZY6R)
    Language English
    Publishing date 2010-09
    Publishing country Netherlands
    Document type Journal Article
    ZDB-ID 2043785-7
    ISSN 1878-1705 ; 1567-5769
    ISSN (online) 1878-1705
    ISSN 1567-5769
    DOI 10.1016/j.intimp.2010.06.002
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  10. Article ; Online: Role of oxidative stress and MAPK signaling in reference moist smokeless tobacco-induced HOK-16B cell death.

    Mitchell, Clint / Joyce, Andrew R / Piper, John T / McKallip, Robert J / Fariss, Marc W

    Toxicology letters

    2010  Volume 195, Issue 1, Page(s) 23–30

    Abstract: The use of smokeless tobacco products is often associated with an oral injury at the site of repeated use. To further our understanding of this injury process, the effect of reference moist smokeless tobacco extract (STE) on cell death, oxidative stress, ...

    Abstract The use of smokeless tobacco products is often associated with an oral injury at the site of repeated use. To further our understanding of this injury process, the effect of reference moist smokeless tobacco extract (STE) on cell death, oxidative stress, and MAPK signaling in a human oral keratinocyte cell line, HOK-16B, was investigated. STE caused dose-dependent cell death and reactive oxygen species (ROS) production within 30 min to 3h of exposure. This same insult enhanced the activity of ERK1/2, JNK1/2, p38 MAPK and ASK1, an upstream activator of JNK1/2 and p38 MAPK. Inhibition of JNK1/2 and to a lesser extent p38 MAPK, but not ERK1/2, suppressed STE-induced cell death. Pretreatment with antioxidants and an iron chelator, deferoxamine suppressed ROS production, ASK1, JNK1/2 and p38 MAPK activation, and reduced cell death after STE exposure. Interestingly, extracellular free iron levels in STE (29.4+/-0.5 microM) were significantly elevated as compared with cell culture medium (4.9+/-0.6 microM) and the addition of extracellular free iron (14, 30 or 70 microM) to HOK-16B cultures (without STE) caused dose-dependent cell death after 3h. Thus, acute exposure to STE leads to HOK-16B cell death in part through oxidative stress via activation of ASK1 and the JNK1/2 and p38 MAPK pathways.
    MeSH term(s) Ascorbic Acid ; Cell Death/drug effects ; Cell Line ; Chromans ; Deferoxamine ; Dose-Response Relationship, Drug ; Gene Expression Regulation/drug effects ; Humans ; Keratinocytes/drug effects ; Keratinocytes/physiology ; MAP Kinase Signaling System/physiology ; Mitogen-Activated Protein Kinase Kinases/metabolism ; Mitogen-Activated Protein Kinases/metabolism ; Oxidative Stress/drug effects ; Time Factors ; Tobacco, Smokeless/toxicity
    Chemical Substances Chromans ; Mitogen-Activated Protein Kinases (EC 2.7.11.24) ; Mitogen-Activated Protein Kinase Kinases (EC 2.7.12.2) ; Deferoxamine (J06Y7MXW4D) ; Ascorbic Acid (PQ6CK8PD0R) ; 6-hydroxy-2,5,7,8-tetramethylchroman-2-carboxylic acid (S18UL9710X)
    Language English
    Publishing date 2010-05-19
    Publishing country Netherlands
    Document type Journal Article
    ZDB-ID 433788-8
    ISSN 1879-3169 ; 0378-4274
    ISSN (online) 1879-3169
    ISSN 0378-4274
    DOI 10.1016/j.toxlet.2010.02.020
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    ab Jg. 2022: Lesesaal (EG)

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