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  • 1
    Keywords: MEDICINE ; biomarker ; CARCINOGEN ; molecular epidemiology ; molecular ; BIOMARKERS ; validation ; EPIDEMIOLOGY ; EXPOSURE
    Type of Publication: Book chapter
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  • 2
    Keywords: CANCER ; EXPRESSION ; DISEASES ; GENE ; GENE-EXPRESSION ; REPAIR ; DAMAGE ; LIPID-PEROXIDATION ; HUMAN-DISEASE ; HYPOMETHYLATION ; METHYLTRANSFERASE ; 3,N-4-ETHENOCYTOSINE ; LIVER DNA ; ADDUCT TYPES
    Abstract: Methylation of cytidine at dCpdG sequences regulates gene expression and is altered in many chronic inflammatory diseases. Inflammation generates lipid peroxidation (LPO) products which can react with deoxycytidine, deoxyadenosine, and deoxyguanosine in DNA to form pro-mutagenic exocyclic etheno-nucleoside residues. Since 5-methyl-2'-deoxycytidine (5mdC) residues exhibit increased nucleophilicity at N3, they should be even better targets for LPO products. We synthesized and characterized 3,N(4)-etheno-5-methyl-2'-deoxycytidine-3'-phosphate and showed that LPO products can indeed form the corresponding etheno-5mdC (epsilon 5mdC) lesion in DNA in vitro. Our newly developed (32)P-postlabeling method was subsequently used to detect epsilon 5mdC lesions in DNA from human white blood cells, lung, and liver at concentrations 4-10 times higher than that observed for etheno adducts on nonmethylated cytidine. Our new detection method can now be used to explore the hypothesis that this DNA lesion perturbs the DNA methylation status
    Type of Publication: Journal article published
    PubMed ID: 22148471
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  • 3
    Keywords: PATTERNS ; smoking ; SMOKERS ; NICOTINE DEPENDENCE ; CIGARETTES ; (-)-MENTHOL
    Abstract: Menthol is the most widely used and the most prominent tobacco additive in tobacco products advertised and marketed by the tobacco industry. Besides its characteristic flavor, it possesses a variety of pharmacological properties facilitating tobacco smoke inhalation and potentiating dependence. These properties of menthol not only favor tobacco initiation and consumption but can also prevent smoking cessation. This article summarizes the effect of menthol as an additive in tobacco products and its effect on tobacco consumption that causes a number of chronic diseases and premature death and, therefore, counteracts tobacco control measures. Currently, there is no legislative regulation in Germany that considers the health hazard, addiction-enhancing and attractiveness-increasing properties of additives permitted in tobacco products. Effective regulation or even a ban could contribute to a reduction of tobacco consumption and, hence, save many people from a long-lasting tobacco dependence.
    Type of Publication: Journal article published
    PubMed ID: 22373857
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  • 4
    Keywords: CANCER ; AGENTS ; Germany ; human ; SUPPORT ; incidence ; POPULATION ; RISK ; MECHANISM ; RISK-FACTORS ; mechanisms ; NO ; HUMANS ; genetics ; risk factors ; smoking ; genotoxicity ; RISK FACTOR ; PRODUCT ; TRANSFORMATION ; POPULATIONS ; TOBACCO ; SQUAMOUS-CELL CARCINOMAS ; ALCOHOL ; mutagenesis ; ALCOHOL-CONSUMPTION ; CONSUMPTION ; education ; ORAL-CANCER ; NECK-CANCER ; YOUNG ; AGENT ; fibrosis ; review ; RE ; PRODUCTS ; INCREASE ; sister chromatid exchange ; ARECA NUT EXTRACT ; BUCCAL MUCOSAL FIBROBLASTS ; CHEWING TOBACCO ; INDEPENDENT RISK-FACTOR ; N-NITROSAMINES ; P53 ONCOPROTEIN ; SUBMUCOUS FIBROSIS
    Abstract: In south-east Asia, Taiwan and Papua New Guinea, smoking, alcohol consumption and chewing of betel quid with or without tobacco or areca nut with or without tobacco are the predominant causes of oral cancer. In most areas, betel quid consists of a mixture of areca nut, slaked lime, catechu and several condiments according to taste, wrapped in a betel leaf. Almost all habitual chewers use tobacco with or without the betel quid. In the last few decades, small, attractive and inexpensive sachets of betel quid substitutes have become widely available. Aggressively advertised and marketed, often claimed to be safer products, they are consumed by the very young and old alike, particularly in India, but also among migrant populations from these areas world wide. The product is basically a flavoured and sweetened dry mixture of areca nut, catechu and slaked lime with tobacco (gutkha) or without tobacco (pan masala). These products have been strongly implicated in the recent increase in the incidence of oral submucous fibrosis, especially in the very young, even after a short period of use. This precancerous lesion, which has a high rate of malignant transformation, is extremely debilitating and has no known cure. The use of tobacco with lime, betel quid with tobacco, betel quid without tobacco and areca nut have been classified as carcinogenic to humans. As gutkha and pan masala are mixtures of several of these ingredients, their carcinogenic affect can be surmised. We review evidence that strongly supports causative mechanisms for genotoxicity and carcinogenicity of these substitute products. Although some recent curbs have been put on the manufacture and sale of these products, urgent action is needed to permanently ban gutkha and pan masala, together with the other established oral cancer-causing tobacco products. Further, education to reduce or eliminate home-made preparations needs to be accelerated
    Type of Publication: Journal article published
    PubMed ID: 15215323
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  • 5
    Keywords: CANCER ; CELLS ; BLOOD ; CELL ; Germany ; human ; IN-VIVO ; VIVO ; DISEASE ; DISEASES ; DNA adducts ; NEW-YORK ; RISK ; METABOLISM ; TISSUE ; ACCURACY ; validation ; ACCUMULATION ; DNA ; MECHANISM ; RISK-FACTORS ; CARCINOGENESIS ; BASE ; BIOMARKERS ; TISSUES ; mechanisms ; BIOLOGY ; MOLECULAR-BIOLOGY ; FORM ; immunohistochemistry ; HUMANS ; ASSAY ; STRESS ; risk factors ; GAS ; mass spectrometry ; TANDEM MASS-SPECTROMETRY ; cancer risk ; DAMAGE ; MASS-SPECTROMETRY ; PRODUCT ; DNA-DAMAGE ; ADDUCTS ; DIETARY ; RISK ASSESSMENT ; OXIDATIVE STRESS ; WHITE BLOOD-CELLS ; MASSES ; PERFORMANCE LIQUID-CHROMATOGRAPHY ; DNA-ADDUCTS ; molecular biology ; molecular ; lipid peroxidation ; PERSISTENT ; review ; RE ; PRODUCTS ; LEADS ; LEVEL ; biomarker ; methods ; DNA ADDUCT ; USA ; CINNAMON LEC RATS ; RISK-FACTOR ; in vivo ; CANCER-RISK ; carcinogenic ; SWITCHING LC/APCI-MS/MS ; HOMEOSTASIS ; 1,N-2-PROPANODEOXYGUANOSINE ADDUCTS ; URINARY-EXCRETION ; lipid ; DIETARY FATTY-ACID ; exocyclic etheno-,Propano-,Malondialdehyde adducts ; P-32 POSTLABELING METHOD
    Abstract: Persistent oxidative stress and excess lipid peroxidation (LPO), induced by inflammatory processes, impaired metal storage, and/or dietary imbalance, cause accumulations and massive DNA damage. This massive DNA damage, along with deregulation of cell homeostasis, leads to malignant diseases. Reactive aldehydes produced by LPO, such as 4-hydroxy-2-nonenal, malondialdehyde, acrolein, and crotonaldehyde, react directly with DNA bases or generate bifunctional intermediates which form exocyclic DNA adducts. Modification of DNA bases by these electrophiles, yielding proinutagenic exocyclic adducts, is thought to contribute to the mutagenic and carcinogenic effects associated with oxidative stress-induced LPO. Ultrasensitive detection methods have facilitated studies of the concentrations of promutagenic DNA adducts in human tissues, white blood cells, and urine, where they are excreted as modified nucleosides and bases. Thus, immunoaffinity-P-32-postlabeling, high-performance liquid chromatography-electrochemical detection, gas chromatography-mass spectrometry, liquid chromatography-tandem mass spectrometry, immunoslotblot assay, and immunohistochemistry have made it possible to detect background concentrations of adducts arising from endogenous LPO products in vivo and studies of their role in carcinogenesis. These background adduct levels in asymptomatic human tissues occur in the order of 1 adduct /10(8) and in organs affected by cancer-prone inflammatory diseases these can be 1 or 2 orders of magnitude higher. In this review, we critically discuss the accuracy of the available methods and their validation and summarize studies in which measurement of exocyclic adducts suggested new mechanisms of cancer causation, providing potential biomarkers for cancer risk assessment in humans with cancer-prone diseases. (c) 2007 Elsevier Inc. All rights reserved
    Type of Publication: Journal article published
    PubMed ID: 17854706
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  • 6
    Keywords: HUMANS ; RISK ; RISKS ; evaluation ; human
    Type of Publication: Book
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  • 7
    ISSN: 1432-1335
    Keywords: Catechin ; Acacta catechu ; Cyanidoanol-3 ; Betel quid
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary In the present study, we report that the betel quid ingredient catechu, its extract and pure principle catechin were nonmutagenic in Salmonella typhimurium TA 100, TA 1535, TA 98, and TA 1538 assays with or without metabolic activation. They also exhibited dose-dependent decreases in mutagenicity of benzo(a)pyrene [B(a)P] and dimethylbenz(a)anthracene (DMBA) in strain TA 98 with metabolic activation. We further report that these compound inhibited activites of cytochrome P-450 and had no effect on glutathione S-transferase but increased the glutathione content in rat liver tissue. Simultaneous treatment of catechin prevented the mutagenic activity of B(a)P and DMBA metabolites in strain TA 98 in the absence of metabolic activation. Pre-and posttreatment of bacteria with catechin had no effect on the mutagenicity of B(a)P and DMBA metabolites. Catechin also inhibited the in vitro binding of 3H-B(a)P metabolites to calf thymus DNA. Catechu extract and catechin inhibited the nitrosation of methylurea by nitrite at pH 3.6 and 30°C. The formation of nitrosomethylurea in the reaction mixture was monitored by measuring the histidine revertants of strain TA 1535 in the absence of metabolic activation. Pre-and post-treatment of catechu extract or catechin had no effect on the mutagenicity of nitrosomethylurea in TA 1535. The nitrosation inhibition by catechin was through scavenging of nitrite observed at pH 3.6. The above study indicates that catechu in betel quid may act as an antimutagen and may suppress the mutagenic potential of other betel quid mutagens.
    Type of Medium: Electronic Resource
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  • 8
    ISSN: 1432-1335
    Keywords: Vitamin A deficiency ; Masheri ; Tumorigenicity ; Mixed-function oxygenases
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The carcinogenicity of long-term feeding of masheri extract to animals in a vitamin-A-sufficient (SLO+) and deficient (SLO−) state was studied in Sprague Dawley rats by feeding daily dose of 3 mg extract over a period of 21 mounths. The phase I activating enzymes, the glutathione (GSH)/glutathione S-transferase (GST) detoxification system, and the hepatic and circulating levels of vitamins A and C were also monitored at 12 and 21 months. It was observed that the phase I enzyme activities were significantly higher in SLO+ than in SLO− rats at both 12 months and 21 months. Moreover, the SLO− masheri-treated animals also showed a decreased in the GSH/GST detoxification system while the reverse was observed in SLO+ group. Masheri extract treatment significantly lowered the hepatic and circulating levels of vitamin A while a concurrent increase was observed in the vitamin C level. The extract was found to be tumorigenic in both the SLO+ and SLO− groups. Benign tumours were observed in the SLO+ group while a high incidence of malignant tumours of the lung were observed in the SLO− group upon treatment with masheri extract.
    Type of Medium: Electronic Resource
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