Disease relevance of Tobacco, Smokeless

• The purpose of this study was to determine whether exposure of chemically transformed golden Syrian hamster oral epidermoid carcinoma cell (HCPC-1) cultures to smokeless tobacco extract (STE) is associated with a decrease in specific angiotensin I-converting enzyme (ACE) activity and whether this decrease potentiates bradykinin-induced cell growth [1].
• Many of the associations observed in this study, notably the risk of soft-tissue sarcoma with smokeless tobacco and medications such as chloramphenicol, deserve further evaluation [2].
• Using the Salmonella/microsome assay system, the mutagenicity of chewing tobacco extracts (CTE) treated with and without sodium nitrite under acidic conditions was examined [3].
• This might maintain the basal level transcription in normal and activates Cdk4 transcription in the initial stage, where as the same role is carried by c-myc in higher stage of chewing tobacco mediated oral cancer development [4].
• The toxicities and oxidative stress-inducing actions of (-)-nicotine and smokeless tobacco extract (STE), containing equivalent amounts of nicotine, were studied [5].

Psychiatry related information on Tobacco, Smokeless

• Treatment of smokeless tobacco addiction with bupropion and behavior modification [6].
• RESULTS: Simple and complex reaction times were not affected by smokeless tobacco use or abstention [7].
• This study evaluated the tobacco use status of 63 subjects seven years after enrollment in a single-intervention smoking cessation study employing smokeless tobacco (SLT) as a nicotine substitute [8].
• Nicotine delivery capabilities of smokeless tobacco products and implications for control of tobacco dependence in South Africa [9].
• Tobacco smoking and alcohol drinking are the principal factors associated with p53 expression in oral squamous cell carcinomas (OSCC) in the west, whereas betel quid chewing and smokeless tobacco are important factors in the east [10].

High impact information on Tobacco, Smokeless

• The following may be concluded about nicotine and smokeless tobacco use: Systemic absorption and levels of nicotine are similar in users of smokeless tobacco and cigarette smokers [11].
• The frequency of anabolic-steroid use was significantly (P < 0.001) associated with the frequency of use in the previous 30 days of cocaine (r = 0.44), injectable drugs, alcohol (r = 0.23), marijuana (r = 0.42), cigarettes (r = 0.25), and smokeless tobacco (r = 0.40) [12].
• Quantitation of metabolites of 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone after cessation of smokeless tobacco use [13].
• Storage effects on chewing tobacco included a 75% increase in nitrite and small increases of nitrosated alkaloids and NNK [14].
• Effect of storage conditions on nitrosated, acylated, and oxidized pyridine alkaloid derivatives in smokeless tobacco products [14].

Biological context of Tobacco, Smokeless

• All tobacco use increased heart rate and blood pressure, with a tendency toward a greater overall cardiovascular effect despite evidence of development of some tolerance to effects of nicotine with use of smokeless tobacco [15].
• These effects were specific because smokeless tobacco extract had no significant effects on vasodilation elicited by nitroglycerin, an endothelium-independent agonist [16].
• The higher heart rates and blood pressures noted during the daytime in smokers and smokeless tobacco users were most likely due to the effects of nicotine [17].
• Hence, in this study, GSH levels, GST activity, GSTM1 genotype and cytogenetic damage were determined using lymphocytes from 114 smokeless tobacco habitues and controls [18].
• To determine the influence of smokeless tobacco (ST) and nicotine on the cytokine phenotype of memory T-cells, splenic mononuclear cells (SPM) were exposed to 1:10(2) or 1:10(3) dilutions of ST extract (ST-SPM), 10 or 100 microg/ml nicotine (NIC-SPM), or medium (CON-SPM) during 4 days of stimulation with anti-CD3 [19].

Anatomical context of Tobacco, Smokeless

• The purpose of this study was to determine whether an aqueous extract of smokeless tobacco (moist snuff) increases clearance of macromolecules from postcapillary venules in the in situ oral mucosa and, if so, whether bradykinin mediated this response [20].
• The frequency of exfoliated cells with micronuclei (MNC) was used to estimate the genotoxic effect of smokeless tobacco (snuff) on the oral mucosa and to follow the response to the administration of beta-carotene (180 mg/week, given twice weekly in 6 capsules of 30 mg each) [21].
• Nicotine, a major component of cigarettes and smokeless tobacco, has toxic effects on endothelium and impairs reactivity of resistance arterioles in response to agonists that stimulate the synthesis and/or release of nitric oxide [22].
• The effects of smokeless tobacco on clinical parameters of inflammation and gingival crevicular fluid prostaglandin E2, interleukin-1 alpha, and interleukin-1 beta [23].
• Formation of carcinogen-DNA adducts in rat oral epithelial cells after treatment with cigarette smoke condensate (CSC) or chewing tobacco in the presence of ethanol was investigated using the 32P-postlabeling procedure [24].

Associations of Tobacco, Smokeless with chemical compounds

• The health hazards known to be caused by cigarette smoking and suspected to be related to chronic nicotine exposure are expected to be a hazard of habitual use of smokeless tobacco [11].
• Smokeless tobacco extract-induced leaky site formation and increase in clearance of FITC-dextran were significantly attenuated by NPC 17647 and Hoe 140 (p < 0.05), two bradykinin B2 receptor antagonists, but not by desArg9,[Leu8]bradykinin, a bradykinin B1 receptor antagonist [20].
• Indomethacin had no significant effects on smokeless tobacco extract-induced responses [20].
• Behavioral counseling, sustained-release bupropion hydrochloride therapy, and nicotine replacement therapy may be safe therapeutic modalities for treatment of smokeless tobacco use [25].
• Plasma nicotine and cotinine concentrations in habitual smokeless tobacco users [26].

Gene context of Tobacco, Smokeless

• Our study provides the first evidence of the constitutive activation of STAT 5-cyclin D1 pathway in chewing tobacco mediated OSCC [27].
• Molecular cloning, isolation and characterisation of ERK3 gene from chewing-tobacco induced oral squamous cell carcinoma [28].
• Modulation of IFN-gamma production from T cells by smokeless tobacco extract (STE) could be a factor in periodontal disease [29].
• The purpose of this study was to examine the effect of smokeless tobacco (ST) on gingival inflammation as assessed clinically and biochemically by gingival crevicular fluid (GCF) levels of PGE2, IL-1 alpha, and IL-1 beta [23].
• No link was found between NHL and usage of smokeless tobacco [30].

Analytical, diagnostic and therapeutic context of Tobacco, Smokeless

• Information about the potential health hazards of nicotine, as well as oral pathology, may be incorporated into educational programs to help discourage the use of smokeless tobacco, with a resultant decrease in the associated cancer risk [11].
• We used chiral stationary phase gas chromatography with nitrosamine-selective detection to determine the enantiomeric composition of NNN and NAT in moist snuff, chewing tobacco, and cigarette tobacco [31].
• Bioassays at lower dose levels as well as biochemical studies are strongly indicated for NNN and NNK since these nitrosamines occur in relatively high amounts in both chewing tobacco and tobacco smoke [32].
• The ineffectiveness of nicotine gum on treatment outcome may be attributed to its similarity with smokeless tobacco [33].
• METHODS: 271 patients (mean age 36 [14] y; 160 men) undergoing diagnostic upper gastrointestinal endoscopy were interviewed regarding symptoms of gastroesophageal reflux, and history of medications, smoking or chewing tobacco and alcohol ingestion [34].

References