The tobacco-specific nitrosamine 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK) is one of the most abundant carcinogens in smokeless tobacco products. NNK uptake by measurement of the urinary metabolites 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanol and its glucuronides (total NNAL) has been reported in many studies, but there are no data in the literature on the percentage of the NNK dose that is converted to NNAL in smokeless tobacco users. In this study, 15 male subjects abstained from tobacco use for 3 weeks before placing 2 g smokeless tobacco between their cheeks and gums for 30 min. They then continued abstinence and collected three consecutive 24-h urine samples. The amount of NNK in the tobacco before and after use was determined along with the amount in expectorated saliva. The NNK dose thus calculated was compared with the amount of total NNAL excreted in the next 72 h. These data, taken together with previous pharmacokinetic data, show that the percent conversion of NNK to total NNAL
Despite improvements in recent years, exposure to SHS remains a significant health risk and public health concern (6). Earlier NHANES evaluations have measured serum cotinine as an index of SHS exposure in the U.S. population and have documented the widespread nature of these exposures. When a cigarette burns, the tobacco-specific nitrosamines partition into mainstream and sidestream smoke and can be measured in the resulting SHS. Thus, nonsmokers are also exposed to tobacco-specific nitrosamines. Consequently, beginning with NHANES 2007 to 2008, we began measuring total urinary NNAL in all participants with the age of ≥6 years. Although concentrations of this carcinogenic metabolite of the tobacco-specific contaminant NNK were much lower than the levels of serum cotinine, we measured total urinary NNAL at or above its detection limit in 41% of nonsmokers, including many young children. In a subgrouping of nonsmokers with elevated levels of serum cotinine indicating relatively substantial ...
Nitrosamines are chemical compounds of the chemical structure R1N(-R2)-N=O, that is, a nitroso group bonded to an amine. Most nitrosamines are carcinogenic. Nitrosamines are used in the manufacture of some cosmetics, pesticides, and in most rubber products.[citation needed] Nitrosamines occur in latex products such as balloons, and in many foods and other consumables. Nitrosamines from condoms are not thought to be of toxicological significance. In foods, nitrosamines are produced from nitrites and secondary amines, which often occur in the form of proteins. Their formation can occur only under certain conditions, including strongly acidic conditions such as that of the human stomach. High temperatures, as in frying, can also enhance the formation of nitrosamines. The presence of nitrosamines may be identified by the Liebermann nitroso reaction (not to be confused with the Liebermann reagent which reacts red or blue in the presence of phenols). Under acidic conditions the nitrite forms nitrous ...
The N-nitrosamine 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK) is a potent lung carcinogen present in tobacco and tobacco smoke. Carbonyl reduction, alpha-carbon hydroxylation (activation) and N-oxidation of the pyridyl ring (detoxification) are the three main pathways of metabolism of NNK. In this study, metabolism of NNK was studied with lung and liver microsomes from F344 rats, Syrian golden hamsters and pigs and cloned flavin-containing monooxygenases (FMOs) from human and rabbit liver. Thermal inactivation at 45 degrees C for 2 min reduced FMO S-oxygenating activity but did not affect N-oxidation of NNK, leading to the conclusion that FMOs are not implicated in the detoxification of NNK. Detoxification of NNK was not increased by n-octylamine or by incubation at pH 8.4, supporting the conclusion that FMOs are not involved in the metabolism of NNK. SKF-525A (1 mM) significantly reduced N-oxidation and alpha-carbon hydroxylation, suggesting that these two pathways were catalyzed by ...
If you wish to reuse any or all of this article please use the link below which will take you to the Copyright Clearance Centers RightsLink service. You will be able to get a quick price and instant permission to reuse the content in many different ways.. ...
The tobacco-specific N-nitrosamines 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK) and 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanol (NNAL), as well as the Areca-derived N-nitrosoguvacoline (NG) were assayed for carcinogenicity in male F344 rats by lifetime administration in the drinking water. Groups of 30 to 80 rats were treated with 0.5 ppm, 1.0 ppm, or 5.0 ppm of NNK; 5.0 ppm of NNAL, 20 ppm of NG, a mixture of 20 ppm of NG and 1 ppm of NNK, and water only in the control group. The approximate total doses of the nitrosamines (mmol/kg of body weight) in these groups were: NNK, 0.073, 0.17, and 0.68; NNAL, 0.69; NG, 4.1; NG and NNK, 4.1 and 0.17. As in previous assays in which NNK was tested by s.c. injection, the lung was its principle target organ. Lung tumor incidences in the 0.5-, 1.0-, and 5.0-ppm groups were nine of 80, 20 of 80, and 27 of 30 compared to six of 80 in the control rats. This trend was significant, P , 0.005. Significant incidences of nasal cavity and liver tumors ...
BS 7115-1 : Determination of Volatile Nitrosamines in Rubber Teats for Feeding Bottles and Babies Dummies Part 1: Dichloromethane Extraction Method
TY - JOUR. T1 - Low ratio of 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanol-glucuronides (NNAL-Gluc)/free NNAL increases urothelial carcinoma risk. AU - Chung, Chi Jung. AU - Lee, Hui Ling. AU - Yang, Hsiu Yuan. AU - Lin, Pinpin. AU - Pu, Yeong Shiau. AU - Shiue, Horng Sheng. AU - Su, Chien-Tien. AU - Hsueh, Yu-Mei. PY - 2011/4/1. Y1 - 2011/4/1. N2 - Cigarette smoking is the most important risk factor for bladder cancer. The compound 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK) and its metabolite 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanol (NNAL) are viewed as biomarkers for cigarette smoking exposure. Therefore, we wanted to explore the effects of these urinary metabolites on urothelial carcinoma (UC) risk. We recruited 127 pairs of UC cases and matched healthy participants for a hospital-based case-control study. Participants completed questionnaires of medical and social information, including smoking history, and provided 50. mL urine samples. Urine samples were analyzed for free ...
We explored the contribution of nitrosamine metabolism to lung cancer in a pilot investigation of genetic variation in CYP2B6, a high-affinity enzymatic activator of tobacco-specific nitrosamines with a negligible role in nicotine metabolism. Previously we found that variation in CYP2A6 and CHRNA5-CHRNA3-CHRNB4 combined to increase lung cancer risk in a case-control study in European American ever-smokers (n = 860). However, these genes are involved in the pharmacology of both nicotine, through which they alter smoking behaviours, and carcinogenic nitrosamines. Herein, we separated participants by CYP2B6 genotype into a high- vs. low-risk group (*1/*1 + *1/*6 vs. *6/*6). Odds ratios estimated through logistic regression modeling were 1.25 (95% CI 0.68-2.30), 1.27 (95% CI 0.89-1.79) and 1.56 (95% CI 1.04-2.31) for CYP2B6, CYP2A6 and CHRNA5-CHRNA3-CHRNB4, respectively, with negligible differences when all genes were evaluated concurrently. Modeling the combined impact of high-risk genotypes yielded odds
Nitrosamine: …aromatic) to N-nitroso compounds (nitrosamines): R2NH + HNO2 → R2N−NO. Some nitrosamines are potent cancer-inducing substances, and their possible formation is a serious consideration when nitrites, which are salts of nitrous acid, are present in foods or pharmaceutical preparations. Tertiary amines give rise to nitrosamines more slowly; an alkyl…
Incidence and mortality rates for lung cancer in the United States are significantly greater in blacks than in whites. This disparity cannot be explained by differences in smoking behavior. We hypothesize that the observed racial differences in risk may be due to differences in the metabolic activation or detoxification of the tobacco-specific lung carcinogen 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK). To test this, different biomarkers of NNK exposure and metabolism, including the urinary metabolite 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanol (NNAL) and the presumed detoxification product [4-(methylnitrosamino)-1-(3-pyridyl)but-1-yl]-beta-O-D-glucosiduronic acid (NNAL-Gluc), were examined along with questionnaire data on lifestyle habits and diet in a metabolic epidemiological study of 34 black and 27 white healthy smokers. Results demonstrated that urinary NNAL-Gluc:NNAL ratios, a likely indicator of NNAL glucuronidation and detoxification, were significantly greater in whites than ...
PubMed Central Canada (PMC Canada) provides free access to a stable and permanent online digital archive of full-text, peer-reviewed health and life sciences research publications. It builds on PubMed Central (PMC), the U.S. National Institutes of Health (NIH) free digital archive of biomedical and life sciences journal literature and is a member of the broader PMC International (PMCI) network of e-repositories.
Smokeless tobacco products have been associated with increased risks of oro-pharyngeal cancers, due in part to the presence of tobacco-specific nitrosamines (TSNAs) such as 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK). These potent carcinogens are formed during tobacco curing and as a result of direct nitrosation reactions that occur in the oral cavity. In the current work we describe the isolation and characterization of a hybridoma secreting a high-affinity, NNK-specific monoclonal antibody. A structurally-related benzoyl derivative was synthesized to facilitate coupling to NNK-carrier proteins, which were characterized for the presence of the N-nitroso group using the Griess reaction, and used to immunize BALB/c mice. Splenocytes from mice bearing NNK-specific antibodies were used to create hybridomas. Out of four, one was selected for subcloning and characterization. Approximately 99% of the monoclonal antibodies from this clone were competitively displaced from plate-bound NNKB conjugates
The tobacco-specific nitrosamines 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK) and N′-nitrosonornicotine (NNN) were tested for carcinogenic activity in Syrian golden hamsters. In Assay A, 30 hamsters were each given 19 s.c. injections of 0.048 mmol of NNK or NNN. In Assay B, 20 hamsters each received 75 s.c. injections of 0.012 mmol of NNK or NNN. Among the NNK-treated hamsters in Assay A, three developed carcinomas of the nasal cavity, and 19 had adenomas and/or adenocarcinomas of the lung. In the NNN group, one hamster developed a lung adenoma, and five had tracheal papillomas. In Assay B, 11 of the NNK-treated hamsters developed carcinomas of the nasal cavity, 16 had lung adenomas and/or adenocarcinomas, and seven had tracheal papillomas; in the NNN group, we recorded only one hamster with a lung adenoma and one with a tracheal papilloma. These findings in the Syrian golden hamster confirm that NNK is a more powerful carcinogen than NNN, as was shown previously in assays with rats ...
DESCRIPTION (provided by applicant): Tobacco-smoking is the single major cause of cancer mortality in the US, and is a risk factor for a number of cancers including lung, upper aero-digestive tract, bladder and pancreas. One of the most powerful carcinogens in tobacco smoke is 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK). NNK is bioactivated to potent electrophiles that react to form methyl and 4-(3-pyridyl)-4-oxobutyl (POB) DNA adducts. Role of methyl-DNA adducts in carcinogenesis have been well characterized and the current paradigm is that methyl- DNA adducts are more important than POB-DNA adducts in the etiology of tobacco-induced cancers. However, recently it was found that O2-POB-dT adduct is the most persistent POB adduct in NNK-treated rodents. Our preliminary results show that O2-POB-dT is inefficiently repaired in human cells and is mutagenic in SOS-induced E. coli and mammalian cells. The objective of this application is to determine the mechanisms by which O2-POB-dT forms ...
The tobacco-specific nitrosamine 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK) is believed to play a role in human lung cancer induced by tobacco smoking. NNK biotransformation may involve the enzymes prostaglandin ...
Figure 3 In vivo effect of phenobarbital pretreatment on NNK teratogenicity in CD-1 mice. Pregnant dams were pretreated with phenobarbital (60 mg/kg i.p.) on GDs 8, 9 and 10, followed by treatment with NNK (100 mg/kg i.p.) on GDs 11 and 12. The number of fetuses or implantations is given in parentheses. *Difference from phenobarbital alone control group (P , .05). †Difference from NNK alone group (P , .05). +Difference from combined saline and phenobarbital alone controls (P = .0083), but not from the phenobarbital alone group (P = .091).. ...
Nitrosamines are carcinogens that require metabolic activation by CYP enzymes in order to exert their carcinogenic effect. Species differences exist in their esophageal carcinogenic potency, with the rat being the most sensitive and the Syrian hamster a resistant species. In the latter, the liver is the main target organ. This difference does not apply to directly acting N-nitroso compounds, suggesting that tissue-specific metabolic activation is involved in hamster esophageal resistance to nitrosamines. We have previously shown that Cytochrome P450 2A3 (CYP2A3) is responsible for N-nitrosodiethylamine activation in the rat esophagus. In order to find a mechanistic explanation for the resistance of hamster esophagus for nitrosamines, we have compared the metabolism of NDEA between esophagus and liver of the hamster. Hamster esophagus is capable of activating NDEA (K-m = 1.02 +/- 0.44 mu M and V-max = 1.96 +/- 0.26 nmol acetaldehyde/min/mg microsomal protein). However, the hamster liver showed a ...
Since direct heating was introduced, the risk of death from smoking has steadily increased.21 Michael Thun and his coworkers attributed these increased risks, in part, to changes in cigarette technology that have occurred since the 1960s. However, in addition to increased levels of TSNAs, there were several other changes in cigarette design that would also be part of the explanation for the observed increased risk of death from smoking. Nevertheless, increased levels of TSNAs cannot be ruled out as part of the explanation for the observed increased risk of death from smoking from the 1960s to 2010.. It might be argued that Thun et als observations of increased risk of death from smoking were observations made in the USA that do not apply to Canada because of substantial differences in the composition of tobacco smoke in the two countries. A closer examination of this possibility is warranted.. There are certainly differences in the composition of tobacco smoke in the two countries. Canadian ...
Why do some smokers get cancer, and others dont. There are likely many factors such as genetics, exposure to environmental pollutants, immune system strength, and others. A new study by Penn State found that the sooner a person smokes a cigarette upon waking in the morning, the more likely he or she is to acquire lung or oral cancer. "We found that smokers who consume cigarettes immediately after waking have higher levels of NNAL -- a metabolite of the tobacco-specific carcinogen NNK -- in their blood than smokers who refrain from smoking a half hour or more after waking, regardless of how many cigarettes they smoke per day," said Steven Branstetter, assistant professor of biobehavioral health. According to Branstetter, other research has shown that NNK (4-(methylnitrosamino)-1-[3-pyridyl]-1-butanone) induces lung tumors in several rodent species. Levels of NNAL (4-(methylnitrosamnino)-1-(3-pyridyl)-1-butanol) in the blood can therefore predict lung cancer risk in rodents as well as in humans. ...
This standard is formulated for the purposes of enforcing the Environment Protection Law of the Peoples Republic of China and Water Pollution Prevention and Control Law of the Peoples Republic of China, protecting the environment, safeguarding the public health, and setting standards for the determination of nitrosamine compounds in waters. This standard specifies the gas chromatography used to determine nitrosamine compounds in surface water, groundwater, industrial sewage, and municipal wastewater. This standard is the original version.. ...
Its relatively OLD NEWS regarding the dangers of nitrosamines in the processed foods we eat. Exposing foods, particularly those with higher nitrite contents, to high temperatures (such as in grilling and frying) cause the nitrites and amines in those foods to transform into nitrosamines. Bacon, hot dogs, other cured meats and certain cheeses that are…
Substances identified in e-cigarette liquids and aerosols include nicotine, solvent carriers (PG and glycerol), tobacco-specific nitrosamines (TSNAs), aldehydes, metals, volatile organic compounds (VOCs), phenolic compounds, polycyclic aromatic hydrocarbons (PAHs), flavorings, tobacco alkaloids, and drugs. Most reviewed studies have evaluated nicotine and impurities in the liquids such as TSNAs and nicotine-related impurities, while other studies have focused on identifying potentially harmful chemicals in the aerosol, such as carbonyl compounds, VOCs, TSNAs, metals, and silicates. Various chemical substances and ultrafine particles known to be toxic, carcinogenic, and/or to cause respiratory and cardiac disease have been identified in e-cigarette aerosols, cartridges, refill liquids, and environmental emissions. Some of the identified TSNAs, aldehydes, metals, VOCs, phenolic compounds, PAHs, and tobacco alkaloids are harmful or potentially harmful constituents." ...
GPRC5A is highly expressed in fetal and adult normal lung tissue suggesting that it plays important roles in the embryonic development, maturation and differentiation of these epithelial organs. A study has shown that mice with knockout of both alleles of this gene developed lung adenomas and adenocarcinomas at 12 months onwards at a much higher rate compared to their wild type littermates. The incidence and size of lung tumors was substantially and significantly increased following exposure of Gprc5a knockout mice to the tobacco-specific carcinogen NNK. Moreover, another study derived a gene expression signature from non-malignant lung epithelial Gprc5a knockout and wild type cells and showed that this signature, indicating GPRC5A loss, was associated with poor survival and prognosis in human lung cancer following cross-comparative analysis of human lung cancer microarray datasets. Mechanistically, loss of Gprc5a was shown to induce constitutive activation of the Nf-kB transcriptional factor ...
Jamasbi, R J. and Perkins, E H., "Immunological characterization of diethyl nitrosamine (den) induced murine forestomach squamous cell carcinomas. Abstr." (1980). Subject Strain Bibliography 1980. 905 ...
The Population Assessment of Tobacco and Health (PATH) Study is a household-based, nationally representative, longitudinal cohort study of approximately 46,000 youth and adults in the United States. The National Institutes of Health (NIH) and the Food and Drug Administration (FDA) announce the availability of restricted-use biomarker data files (Biomarker RUF) from the first wave of the PATH Study, in addition to the launch of the Studys new Biospecimen Access Program that provides the research community with access to urine, serum, and plasma collected from adult study participants during Wave 1.. With over 21,000 adult study participants providing a urine specimen and over 14,000 providing a blood specimen (most of whom also provided a urine specimen) in Wave 1, the newly released Biomarker RUF contain the results of laboratory analyses for a subset of the specimens. The files include measurements of arsenic, creatinine, metals, polycyclic aromatic hydrocarbons, tobacco-specific nitrosamines, ...
Structure, properties, spectra, suppliers and links for: 1-{[(4R,7S,10R,13S,16R,19S)-19-Amino-7-(2-amino-2-oxoethyl)-10-(3-amino-3-oxopropyl)-13-benzyl-1.
(3-Amino-2-oxopropyl)phosphonous acid | C3H8NO3P | CID 24905541 - structure, chemical names, physical and chemical properties, classification, patents, literature, biological activities, safety/hazards/toxicity information, supplier lists, and more.
NNA was tested by intraperitoneal injection in female mice of one strain at one dose level only. Although the incidence of lung adenomas in treated mice exceeded those in controls, the experiment does not allow an evaluation of the carcinogenicity of NNA.. No data were available on mutagenic or related effects of NNA ...
Rats were fed N-nitrosomorpholine (NNM) at low or high concentrations for 6 or 12 weeks. Both NNM schedules resulted in development of hepatomas. During the early stages of hepatoma induction, liver histotoxic patterns depended only on the dose of carcinogen employed. Necrosis of hepatocytes and proliferation of small, oval-shaped cells occurred when high doses of NNM were applied. Parallel to the proliferation of oval-shaped cells, resurgence of alpha1-fetoprotein (AFP) in rat sera was observed and production of this protein was confined to the oval-shaped cells as shown by immunoperoxidase staining. During proliferation of bile duct epithelium, induced by galactosamine injections, those cells could also stain for AFP, and proliferation of oval-shaped cells concomitant with intracellular AFP staining resulted from restitution of heavily damaged liver. At the stage of malignant conversion, distinct AFP-staining nodules were localized which consisted of neoplastic hepatocytes ...
Comments:input packing wanted or destination,payment terms and other messages (we prefer you directly send your request to [email protected] or [email protected] for backup ...
Comments:input packing wanted or destination,payment terms and other messages (we prefer you directly send your request to [email protected] or [email protected] for backup ...
SCI, SSCI ve AHCI dışındaki indeks ve özler tarafından taranan dergilerde yayımlanan teknik not, editöre mektup, tartışma, vaka takdimi ve özet türünden yayınlar dışındaki makale ...
Don Lehman is an industrial designer who strives to surround the products he designs with an array of touch points and media to create rich experiences for clients and consumers. Having worked in both boutique design studios and Fortune 500 companies has given him a unique perspective on what it takes to bring successful products and services to market. Don has been recognized by the IDSA, CES Innovation, and his design for the Contigo Autoseal Travel Mug was named by Bloomberg/BusinessWeek as one of the "50 Coolest Designs of the 21st Century ...
Cigarette smoke is a complex mixture containing, among other chemicals, pyridine alkaloids and N-nitrosamines. Carcinogenic tobacco-specific N-nitrosamines, N-nitrosodimethylamine (NDMA) and 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK), are both activated by cytochrome P450 (CYP) 2E1 in rats. Previous reports indicate that nicotine and the main nicotine metabolite, cotinine, reduce the mutagenicity of both NNK and NDMA in Salmonella typhimurium. To study the mechanism of this effect, we examined inhibition of CYP 2E1 activity, as assessed by p-nitrophenol (pNP) hydroxylation, by nicotine, cotinine, and an aqueous cigarette tar extract (ACTE) in human 2E1-expressing microsomes. At all substrate concentrations (0-1.25 mM) nicotine was a significantly more potent inhibitor of CYP 2E1 activity compared to cotinine. Estimated Ki values for nicotine and cotinine (both at 10 mM) were 13 mM (2 mg/ml) and 308 mM (54 mg/ml) respectively. The Ki for ACTE was 0.2 mg/ml at a concentration of 0.32 mg/ml.
In this application note, we describe a UPLC-MS/MS method for TSNA analysis in tobacco products that has been developed based on the CORESTA standard (CRM-72), and provides further improvements in sensitivity, linear dynamic range, sample workflow, and overall analysis throughput.
This Technical Report aims to contribute to providing general advice on strategies that can be adopted to minimize the likelihood of N-nitrosamine formation in cosmetic products and provide a description of the analytical methodologies available for the reliable determination of N-nitrosamines in cosmetic products. It also seeks to provide some insight into the relevance and limitations of each of the methods described and finally provide an analytical approach for the analysis of N-nitrosamines in cosmetic products and raw materials. This Technical Report covers the reduction or elimination of adventitious nitrite sources, reduction or elimination of secondary amino sources, incorporation of inhibitors to N-nitrosamine formation and analytical methodologies for total N-nitroso compounds and specific methods for N-nitrosodiethanolamine (NDELA ...
Know the Autoimmune Triggers!. One of the most common questions I get is…"How did I develop this autoimmune condition?" Well…its pretty much genetics and the environment. Its a matter of what came first, the chicken or the egg? We all know that genetically, you may be at risk for developing certain problems and/or conditions. If your mom had a thyroid condition, if your grandmother had a thyroid condition, you probably have a thyroid condition too, so its genetic.. Then there are environmental factors, one of them being chemicals such as cigarette smoke. There are over 519 chemicals in cigarettes. Here are just a few of them…. TSNAs: Tobacco-specific N-nitrosamines (TSNAs) are known to be some of the most potent carcinogens present in smokeless tobacco, snuff and tobacco smoke.. Benzene: Benzene can be found in pesticides and gasoline. It is present in high levels in cigarette smoke and accounts for half of all human exposure to this hazardous chemical.. Pesticides: Pesticides are used ...
The protective effect of polyphenol-rich haskap berry extracts against tobacco-specific nitrosamine ketone (NNK)-induced DNA damage was studied in vitro. Normal lung epithelial BEAS-2B cells were exposed to NNK, and to its precursor, 4-[(acetoxymethyl) nitrosamino]-1-(3-pyridyl)-1-butanone (NNKOAc), to induce DNA damage. Polyphenols present in haskap berries were extracted using ethanol and water, separately. Quercetin-3-O-glucoside (Q3G) and cyanidin-3-O-glucoside (C3G) were used as the reference compounds. BEAS-2B cells were pre-incubated with non-cytotoxic concentrations of haskap extracts, Q3G, and C3G separately, and investigated for their protective effects against NNK- and NNKOAc-induced DNA damage. Pre-incubation of BEAS-2B cells with haskap extracts, Q3G, and C3G, significantly suppressed the NNK- and NNKOAc-induced DNA strand breaks, and intracellular reactive oxygen species generation. The protective effect of haskap extracts could be related to their polyphenol content and high ...
Exposure to tobacco-specific nitrosamines (TSNA) and polycyclic aromatic hydrocarbons (PAH) is recognized to play an important role in the development of oral/head and neck squamous cell cancer (HNSCC). We recently reported higher levels of TSNA-associated DNA adducts in the oral cells of smokers with HNSCC as compared with cancer-free smokers. In this study, we further investigated the tobacco constituent exposures in the same smokers to better understand the potential causes for the elevated oral DNA damage in smokers with HNSCC. Subjects included cigarette smokers with HNSCC (cases, n = 30) and cancer-free smokers (controls, n = 35). At recruitment, tobacco/alcohol use questionnaires were completed, and urine and oral cell samples were obtained. Analysis of urinary 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanol (NNAL) and N-Nitrosonornicotine (NNN; TSNA biomarkers), 1-hydroxypyrene (1-HOP, a PAH), cotinine, 3′-hydroxycotinine, and the nicotine metabolite ratio (NMR) were performed. Cases ...
BACKGROUND: Previous epidemiologic studies found inconsistent results for the association between red meat intake, nitrosamines [NDMA: N-nitrosodimethylamine, and ENOC (endogenous nitroso compounds)], and the risk of bladder cancer. We investigated the association between red meat consumption, dietary nitrosamines, and heme iron and the risk of bladder cancer among participants of the European Prospective Investigation into Cancer and Nutrition (EPIC). METHODS: Data on food consumption and complete follow-up for cancer occurrence were available for a total of 481,419 participants, recruited in 10 European countries. Estimates of HRs were obtained by proportional hazard models, stratified by age at recruitment, gender, and study center and adjusted for total energy intake, smoking status, lifetime intensity of smoking, duration of smoking, educational level, and BMI. RESULTS: After a mean follow-up of 8.7 years, 1,001 participants were diagnosed with bladder cancer. We found no overall association
This has been reported more frequently with the use of agents with prolonged half-lives. phentermine 30mg without prescription can phentermine cause erectio
Most of the available data on the occurrence of N-nitrosamines (NA) in processed meat products have been generated in the 1980s and 1990s and especially data on the occurrence of non-volatile NA (NVNA) are scarce. Therefore we have studied the levels of volatile nitrosamines (VNA) and NVNA in processed meat products on the Danish market (N = 70) and for comparison also products on the Belgian market (N = 20). The effect of heat treatment on the NA levels, in selected samples, was also studied, in order to enable an evaluation of how preparation before consumption affects the levels of NA. For the Danish products the mean levels of the VNA were generally low (≤0.8 μg kg−1), whereas the mean levels of the NVNA were considerably higher (≤118 μg kg−1). Slightly higher mean levels were indicated for the Belgian products (i.e. VNA ≤1.5 μg kg−1 and NVNA ≤270 μg kg−1). The sums of VNA were higher than 10 μg kg−1 for one Danish sample and two Belgian samples. Levels of up to 2000 ...
Abanobi SE, Farber E, Sarma DSR (1979) Persistence of DNA damage during development of liver angiosarcoma in rats fed dimethylnitrosamine. Cancer research, 39:1592 1596.. Adams JD, O Mara-Adams KJ, Hoffmann D (1987) Toxic and carcinogenic agents in undiluted mainstream smoke and side stream smoke of different types of cigarettes. Carcinogenesis, 8(5):729 731.. Agrelo C, Phillips JC, Lake BG, Longland RC, Gangolli SD (1978) Studies on the gastrointestinal absorption of N-nitrosamines: effect of dietary constituents. Toxicology, 10:159 167.. Alexandrov VA (1968) Blastomogenic effect of dimethylnitrosamine on pregnant rats and their offspring. Nature, 218:280 281.. Alexandrov VA (1974) [Embryotoxic and transplacental oncogenic action of symmetrical dialkylnitrosamines on the progeny of rats.] Bulletin of experimental biology and medicine, 78:1308 1310 (in Russian) [cited in ATSDR, 1989].. Althoff J, Pour P, Grandjean C, Marsh S (1977) Transplacental effects of nitrosamines in Syrian hamsters. ...
Exposures to volatile nitrosamines were measured at 24 rubber manufacturing plants from 1992 to 1995. A total of 709 exposure measurements were taken in general areas or personal breathing zones to estimate exposure according to production types seals, joints, tyres, gloves, etc. and production steps, from mixing to storage. Five different...
Our results reveal that urinary total NNAL levels were more than 4-fold higher among smokers in Singapore than in Shanghai. One might wonder if the lower levels of total NNAL in Shanghai versus Singapore smokers were the result of degradation of NNAL in urine during storage. Shanghai samples were collected during 1986-1989 while the Singapore samples were collected during 1994-2005. We believe this is an unlikely scenario. Our experimental data have shown that total NNAL is stable for at least 4 years in urine samples stored at -20 °C. Further, mean total NNAL (0.74 pmol/mg Cr) based on samples collected during the early phase of the Singapore Study (1994-1999) was comparable to that (0.65 pmol/mg Cr) based on samples collected later (2000-2005) (P = 0.70). We speculate that the varying levels of urinary total NNAL between smokers in Shanghai versus Singapore may stem from the considerably lower concentrations of NNK in local Chinese brands (western, imported brands were unavailable in Shanghai ...
Carcinogenesis, Volume 27, Issue 1, 2006, pages 137-145. Azzi, C., Zhang, J., Purdon, C.H., Chapman, J.M., Nitcheva, D., Hébert, J.R., & Smith, E.W. (2006). Permeation and reservoir formation of 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK) and benzo[a]pyrene (B[a]P) across porcine esophageal tissue in the presence of ethanol and menthol. Carcinogenesis, 27(1), 137-145. doi: 10.1093/carcin/bgi173. © 2005 Oxford University Press.. ...
This review document consists of two parts. The first is a review of the published information about the formation of nitrosamines in vulcanisates and also legislative and environmental considerations. The second part is a summary of the collaborative study carried out at Rapra.
This review document consists of two parts. The first is a review of the published information about the formation of nitrosamines in vulcanisates and also legislative and environmental considerations. The second part is a summary of the collaborative study carried out at Rapra.
Reason #1: "Safety concerns." KP mentions a six year old FDA study that reported traces of diethylene glycol and tobacco-specific nitrosamines in some e-cig liquid samples. As I explained, "the FDA tested e-cigarettes for TSNAs using a questionable sampling regimen, using methods that were so sensitive that the results may have no possible significance to users. The agency failed to report specific levels of these contaminants, and it has failed to conduct similar testing of nicotine medicines that have been sold in the U.S. for over 20 years." Not only is the study outdated and irrelevant, subsequent studies have failed to find diethylene glycol in e-cig liquids ...