Toxic and carcinogenic agents in dry and moist stuff

Hoffmann, Dirk W.; Actams, JD; Lisk, Donald J.

doi:10.1016/0378-8741(88)90069-4

Cited by 43 publications

(79 citation statements)

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“…The reasons for this difference are uncertain. Snus contains high amounts of nitrate [27], which is associated with an increased nitrite formation in the oral cavity and further to formation of nitric oxide in the stomach [28][29][30]. In contrast, cigarette smoking seems to be related to reduced levels of nitrite in saliva [31].…”

Section: Helicobacter Pylori and Serologymentioning

confidence: 99%

Section: Helicobacter Pylori and Serology 16mentioning

confidence: 99%

“…The nitric oxide generating solution also increased esophageal acid exposure [35]. Whether swallowed alkaline tobacco-contaminated saliva, comprising tobacco specific nitrosamine compounds [27], has any role in the development of esophagitis is unclear.Juice from snus contains high amounts of nitrate which can be reduced to nitrite in the oral cavity [28][29][30]. When saliva, including dietary nitrate, converted to nitrite, meets acidic gastric juice, the nitrite is converted to nitrous acid, nitrosative species and nitric oxide [29,30,36].…”

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confidence: 99%

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Use of tobacco products and gastrointestinal morbidity: an endoscopic population-based study (the Kalixanda study)

et al. 2010

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There is little knowledge regarding the relationship between gastrointestinal symptoms and snus. The nicotine intake is usually higher than in smokers, and a great deal of tobacco juice contaminated saliva is swallowed during use. In a Swedish cross-sectional study of symptoms in 130,000 construction workers, smokers reported "ulcer-like" dyspepsia three times as often 5 as the non tobacco users, while snus users reported significantly fewer symptoms than both smokers and non tobacco users [10].It has been shown both in studies on patients and in population-based studies that smoking is a risk factor for peptic ulcer disease (PUD) [8,11], but there are no data concerning snus on this issue. Data from the US show that cigarette smokers have a markedly increased risk for gastric cancer and that use of more than one tobacco product increases the risk in men [12].Male users of smokeless or chewing tobacco have also been shown in US prospective studies to have higher death rates from all causes compared with non-users (CPS-I and II studies) and also higher death rates from cancer of the gastrointestinal tract overall (CPS-I study), but separate data on the upper gastrointestinal tract were not shown [13].Although there is extensive exposure to swallowed tobacco juice contaminated saliva, and high serum levels of nicotine and nitrites, there have been no studies in terms of oesophageal or gastric histology or Helicobacter pylori infection in snus users.The aim of the study was to investigate whether smoking cigarettes and snus use are associated with gastrointestinal symptomatology, macroscopic findings on endoscopy or histological signs of inflammation or cancer risk markers in the esophagus or stomach, including the prevalence of Helicobacter pylori. MATERIALS AND METHODS SettingThe Kalixanda study setting consisted of two neighbouring communities in Northern Sweden (Kalix and Haparanda) with 28,988 inhabitants (December 1998). The distribution of age and sex was similar to the national average in Sweden in both communities; although proportion of unemployment, income, and the proportion with a higher education were slightly lower [14]. ParticipantsBy using the computerized national population register, covering all citizens in the two communities by date of birth order, a representative stratified sample was generated. Every seventh adult (n=3,000) from the target population (18-80 years of age, n=21,610 in September 1998) was drawn. The sampled subjects were given an identification number (1-3,000) in a random order [14]. Study design and logisticsThe original study population (n=3,000) was invited by mail to take part. The invitation included information of the study design and of the aims of the study and a validated questionnaire, the Abdominal Symptom Questionnaire (ASQ) to be returned by mail [15]. Up to two remainders were sent when necessary; 140 subjects were unavailable at the time for invitation, thus 2,860 of the original study population were eligible for inclusion [14]. The overall response rate was 7...

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Section: Helicobacter Pylori and Serologymentioning

confidence: 99%

Section: Helicobacter Pylori and Serology 16mentioning

confidence: 99%

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confidence: 99%

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Use of tobacco products and gastrointestinal morbidity: an endoscopic population-based study (the Kalixanda study)

et al. 2010

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“…The extract was prepared according to the method of Oh et al (19) as described in previous studies in our laboratory and reports in the literature (12,15,16,23,28). Ten grams of smokeless tobacco were mixed with 100 ml saline and incubated at 37°C for 2 h. The mixture was then centrifuged at 450 g for 10 min.…”

Section: General Methodsmentioning

confidence: 99%

“…Ten grams of smokeless tobacco were mixed with 100 ml saline and incubated at 37°C for 2 h. The mixture was then centrifuged at 450 g for 10 min. The supernatant was collected and centrifuged at 13,000 g for 1 h. After the pH was adjusted to 7.4 with 0.1 N HCl, the resulting supernatant, designated arbitrarily as 10.0% smokeless tobacco extract (12,15,16,19,23,28), was filtered through a Millipore filter (pore size 0.45 µm), divided into 2-ml samples, snap frozen in liquid nitrogen, and stored at 270°C until used.…”

Section: General Methodsmentioning

confidence: 99%

Purified ACE attenuates smokeless tobacco-induced increase in macromolecular efflux from the oral mucosa

Gao

Suzuki

Olopade

et al. 1997

Journal of Applied Physiology

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Purified ACE attenuates smokeless tobacco-induced increase in macromolecular efflux from the oral mucosa. J. Appl. Physiol. 83(1): 74-81, 1997.-The purpose of this study was to determine whether purified angiotensin I-converting enzyme (ACE) attenuates smokeless tobacco extract (STE)-induced increase in macromolecular efflux from the in situ oral mucosa. By using intravital microscopy, we found that suffusion of an aqueous extract of smokeless tobacco elicited significant concentration-dependent leaky site formation and increase in clearance of fluorescein isothiocyanate-labeled dextran (mol mass, 70 kDa) from the hamster cheek pouch (P , 0.05). Suffusion of purified rabbit lung ACE significantly attenuated these responses in a concentration-dependent fashion (P , 0.05). These effects were specific because purified ACE also significantly attenuated the increase in macromolecular efflux elicited by bradykinin, which is produced in the cheek pouch during suffusion of STE, but did not attenuate the increase elicted by adenosine. Moreover, suffusion of heat-inactivated purified ACE and purified superoxide dismutase had no significant effects on STE-and bradykinin-induced responses. Collectively, these data suggest that exogenous ACE attenuates STE-induced increase in macromolecular efflux from the in situ oral mucosa, in part, by promoting local bradykinin catabolism.

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Mutations of thep53 gene in oral squamous-cell carcinomas from sudanese dippers of nitrosamine-rich toombak and non-snuff-dippers from the Sudan and Scandinavia

et al. 1999

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Using PCR-SSCP/DNA sequencing methods, we analyzed 14 oral squamous-cell carcinomas (OSCCs) and 8 premalignant oral lesions from different Sudanese patients for prevalence of mutations in exons 5 to 9 of the p53 gene in relation to toombak-dipping status. OSCCs (14 from Sudan, 28 from Scandinavia), and 3 pre-malignant oral lesions from Sudanese non-dippers were used as controls. A statistically significant increased incidence in mutations of the p53 gene was found in OSCCs from toombak dippers (93%; 13/14), as compared with those from non-dippers in Sudan (57%; 8/14) and in Scandinavia (61%; 17/28) respectively. In OSCCs from dippers, mutations were found in exons 5 to 9, while in those from non-dippers they were found in exons 5, 7, 8, 9, and no mutations were found in exon 8 in any of the OSCCs from Sudan. Certain types of mutations, however, were similar with respect to exposure to toombak. OSCCs from dippers showed 15 transversions, 9 transitions, 3 insertions and one deletion, compared with 7 transversions, 2 transitions and one deletion found in OSCCs from Sudanese non-dippers, and 9 transversions, 17 transitions and 2 insertions found in those from non-dippers in Scandinavia. No mutations were found in any of the non-malignant oral lesions in relation to dipping or non-dipping status. These findings suggest that (i) the use of toombak plays a significant role in induction of increased p53 gene mutations, (ii) mutations observed were similar to those induced by tobacco-specific N-nitrosamines (TSNAs) in experimental animal models and those already reported in toombak dippers, (iii) types of mutations associated with TSNAs were similar in the exposed and the control groups, (iv) a novel mutation in exon 6 was found in the OSCCs from toombak dippers, (v) the p53 exons 5 (codon 130), 6 (codons 190, 216) and 7 (codons 229, 249, 252) mutations are probable hot spots for toombak-related OS-CCs. Further studies are necessary to validate the increased incidence and exon locations of the p53-gene mutations as a biomarker of malignant transformation in populations in which the oral use of tobacco is habitual.

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Toxic and carcinogenic agents in dry and moist stuff

Cited by 43 publications

References 0 publications

Use of tobacco products and gastrointestinal morbidity: an endoscopic population-based study (the Kalixanda study)

Use of tobacco products and gastrointestinal morbidity: an endoscopic population-based study (the Kalixanda study)

Purified ACE attenuates smokeless tobacco-induced increase in macromolecular efflux from the oral mucosa

Mutations of thep53 gene in oral squamous-cell carcinomas from sudanese dippers of nitrosamine-rich toombak and non-snuff-dippers from the Sudan and Scandinavia

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