acetaldehyde/dental caries

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Increased acetaldehyde production by mouthwashings from patients with oral cavity, laryngeal, or pharyngeal cancer.

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Excessive ethanol consumption is associated with an increased risk of oral cavity, laryngeal, and pharyngeal cancer. Ethanol has been shown to be oxidized to acetaldehyde by microflora of the upper respiratory tract. As a highly toxic and reactive compound, acetaldehyde of microbial origin has been

A single sip of a strong alcoholic beverage causes exposure to carcinogenic concentrations of acetaldehyde in the oral cavity.

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The aim of this study was to explore oral exposure to carcinogenic (group 1) acetaldehyde after single sips of strong alcoholic beverages containing no or high concentrations of acetaldehyde. Eight volunteers tasted 5 ml of ethanol diluted to 40 vol.% with no acetaldehyde and 40 vol.% calvados

Role of yeasts in the salivary acetaldehyde production from ethanol among risk groups for ethanol-associated oral cavity cancer.

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BACKGROUND Acetaldehyde, the first metabolite of alcohol, has been proposed to be the carcinogenic substance behind ethanol-related oral cancers. High levels of acetaldehyde are formed from ethanol in saliva by the oral flora, but so far the role of certain microbial species responsible for this

Alcohol-Derived Acetaldehyde Exposure in the Oral Cavity.

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Alcohol is classified by the International Agency for Research on Cancer (IARC) as a human carcinogen and its consumption has been associated to an increased risk of liver, breast, colorectum, and upper aerodigestive tract (UADT) cancers. Its mechanisms of carcinogenicity remain unclear and various

Increased salivary acetaldehyde levels in heavy drinkers and smokers: a microbiological approach to oral cavity cancer.

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The pathogenetic mechanisms behind alcohol-associated carcinogenesis in the upper digestive tract remain unclear, as alcohol is not carcinogenic. However, there is increasing evidence that a major part of the tumour-promoting action of alcohol might be mediated via its first, toxic and carcinogenic

Buccal tablets containing cysteine and chlorhexidine for the reduction of acetaldehyde levels in the oral cavity.

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There is growing evidence that a large proportion of upper digestive tract tumors are ascribable to heavy alcohol drinking and tobacco consumption. The cancer-promoting action of ethanol is mediated by acetaldehyde, its first metabolite, also derived from the bacterial oxidation of alcohol by the

Correction: Alessia Stornetta et al. Alcohol-Derived Acetaldehyde Exposure in the Oral Cavity. Cancers 2018, 10, 20.

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The authors would like to make a correction to their published paper[...].

Xylitol inhibits carcinogenic acetaldehyde production by Candida species.

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Acetaldehyde is a highly toxic and mutagenic product of alcohol fermentation and metabolism which has been classified as a Class I carcinogen for humans by the International Agency for Research on Cancer of the World Health Organisation (WHO). Many Candida species representing oral microbiota have

A shared binding site for NAD+ and coenzyme A in an acetaldehyde dehydrogenase involved in bacterial degradation of aromatic compounds.

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The meta-cleavage pathway for catechol is a central pathway for the bacterial dissimilation of a wide variety of aromatic compounds, including phenols, methylphenols, naphthalenes, and biphenyls. The last enzyme of the pathway is a bifunctional aldolase/dehydrogenase that converts

Subchronic inhalation of mixtures of cigarette smoke constituents in Xpa-/-p53+/- knock-out mice: a comparison of intermittent with semi-continuous exposure to acetaldehyde, formaldehyde, and acrolein.

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We investigated whether inhaling peak concentrations of aldehydes several times daily is more damaging than semi-continuously inhaling low-dose aldehydes. We exposed Xpa-/-p53+/- knock-out mice either intermittently or semi-continuously to mixed acetaldehyde, formaldehyde, and acrolein. The

High acetaldehyde levels in saliva after ethanol consumption: methodological aspects and pathogenetic implications.

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Chronic ethanol ingestion leads to an enhanced risk of upper gastrointestinal tract cancer. Although many hypotheses for the tumor promoting effect of alcohol exist, the pathogenetic mechanisms remain unclear since alcohol in itself is not carcinogenic. Acetaldehyde, the first metabolite of ethanol,

Acetaldehyde production and other ADH-related characteristics of aerobic bacteria isolated from hypochlorhydric human stomach.

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BACKGROUND Acetaldehyde is a known local carcinogen in the digestive tract in humans. Bacterial overgrowth in the hypochlorhydric stomach enhances production of acetaldehyde from ethanol in vivo after alcohol ingestion. Therefore, microbially produced acetaldehyde may be a potential risk factor for

Wine Consumption and Oral Cavity Cancer: Friend or Foe, Two Faces of Janus

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The health benefits of moderate wine consumption have been extensively studied during the last few decades. Some studies have demonstrated protective associations between moderate drinking and several diseases including oral cavity cancer (OCC). However, due to the various adverse effects related to

Multicomponent trace-gas analysis by three intracavity photoacoustic cells in a CO laser: observation of anaerobic and postanaerobic emission of acetaldehyde and ethanol in cherry tomatoes.

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Three serial photoacoustic cells are employed within the cavity of a liquid-nitrogen-cooled CO laser to monitor on-line trace-gas concentrations. Multicomponent gas analysis is performed on sequential repetitive measurements of ethylene, acetaldehyde, CO2, ethanol, and H2O. To demonstrate the high

Synthesis of molecularly imprinted monolithic fibers for solid-phase microextraction of acetaldehyde from head-space of beverages stored in PET bottles.

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Molecularly imprinted monolithic fibers were synthesized and evaluated for solid-phase microextraction (SPME) of acetaldehyde from head-space of beverages stored in poly(ethylene terephthalate) (PET) bottles. The fibers were prepared by co-polymerization of methacrylic acid and ethylene glycole

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