acetaldehyde/zhubný nádor

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Benzo[a]pyrene, aflatoxine B₁ and acetaldehyde mutational patterns in TP53 gene using a functional assay: relevance to human cancer aetiology.

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Mutations in the TP53 gene are the most common alterations in human tumours. TP53 mutational patterns have sometimes been linked to carcinogen exposure. In hepatocellular carcinoma, a specific G>T transversion on codon 249 is classically described as a fingerprint of aflatoxin B(1) exposure.

Short-term salivary acetaldehyde increase due to direct exposure to alcoholic beverages as an additional cancer risk factor beyond ethanol metabolism.

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BACKGROUND An increasing body of evidence now implicates acetaldehyde as a major underlying factor for the carcinogenicity of alcoholic beverages and especially for oesophageal and oral cancer. Acetaldehyde associated with alcohol consumption is regarded as 'carcinogenic to humans' (IARC Group 1),

Reduction of oral acetaldehyde levels using a controlled-release chlorhexidine chip as a prevention strategy against upper digestive tract cancer.

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Increasing evidence indicates a strong relationship exists between harmful habits like smoking and alcohol drinking and upper digestive tract cancer. In addition, smokers and alcohol drinkers also exhibit high salivary levels of carcinogenic acetaldehyde, the first metabolite of alcohol. This

Ethanol-induced oxidative stress and acetaldehyde formation in rat mammary tissue: potential factors involved in alcohol drinking promotion of breast cancer.

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Recent studies from our laboratory provided evidence that part of the carcinogenic effects of ethanol consumption might be related to its in situ metabolism at cytosolic and microsomal levels, to the mutagen acetaldehyde and to hydroxyl and 1-hydroxyethyl radicals. In this work, we report on our

PPARalpha and PPARbeta are differentially affected by ethanol and the ethanol metabolite acetaldehyde in the MCF-7 breast cancer cell line.

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The activity and/or the level of the peroxisome proliferator-activated receptors (PPARs) in liver and oligodendrocytes are regulated by ethanol. Despite the association between ethanol consumption and breast cancer risk, and the increasing evidence for an involvement of PPARs in some cancers, there

Cancer induction in mice with acetaldehyde methylformylhydrazone of the false morel mushroom.

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Acetaldehyde methylformylhydrazone (AMFH), which occurs up to 0.3% in one of the edible false morel mushrooms, Gyromitra esculenta, was administered to noninbred Swiss mice in propylene glycol in 52 weekly intragastric instillations as 100 micrograms/g body weight. The treatment induced tumors of

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

Evaluation of potential salivary acetaldehyde production from ethanol in oral cancer patients and healthy subjects.

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BACKGROUND Acetaldehyde has been implicated as a major factor in oral carcinogenesis associated with alcohol consumption. In this study, saliva samples from oral cancer patients and healthy individuals were incubated in vitro with ethanol in order to investigate factors which can influence salivary

Cytosolic xanthine oxidoreductase mediated bioactivation of ethanol to acetaldehyde and free radicals in rat breast tissue. Its potential role in alcohol-promoted mammary cancer.

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Epidemiological evidence links alcohol intake with increased risk in breast cancer. Not all the characteristics of the correlation can be explained in terms of changes in hormonal factors. In this work, we explore the possibility that alcohol were activated to acetaldehyde and free radicals in situ

Rat ventral prostate xanthine oxidase bioactivation of ethanol to acetaldehyde and 1-hydroxyethyl free radicals: analysis of its potential role in heavy alcohol drinking tumor-promoting effects.

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The ability of the ventral prostate cytosolic fractions to biotransform ethanol to acetaldehyde and 1-hydroxyethyl (1HEt) radicals was tested. Acetaldehyde formation was determined by GC-FID analysis in the head space of incubation mixtures. 1HEt was determined by spin trapping with PBN followed by

Interrelationship between alcohol, smoking, acetaldehyde and cancer.

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In industrialized countries alcohol and tobacco are the main risk factors of upper digestive tract cancer. With regard to the pathogenesis of these cancers, there is strong epidemiological, biochemical and genetic evidence supporting the role of the first metabolite of alcohol

Genetic-epidemiological evidence for the role of acetaldehyde in cancers related to alcohol drinking.

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Alcohol drinking increases the risk for a number of cancers. Currently, the highest risk (Group 1) concerns oral cavity, pharynx, larynx, esophagus, liver, colorectum, and female breast, as assessed by the International Agency for Research on Cancer (IARC). Alcohol and other beverage constituents,

Acetaldehyde burst protection of ADH1B2 against alcoholism: an additional hormesis protection against esophageal cancer*s following alcohol consumption?

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This account of recent work presented at the 4th International Symposium on Alcohol Pancreatitis and Cirrhosis reports animal studies aimed at determining the role of the "acetaldehyde burst," generated shortly upon ethanol intake, as the mechanism of protection against alcoholism conferred by the

Acetaldehyde-induced interleukin-1beta and tumor necrosis factor-alpha production is inhibited by berberine through nuclear factor-kappaB signaling pathway in HepG2 cells.

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Alcoholic liver disease (ALD) is one of the most common liver diseases in the world. Increased levels of proinflammatory cytokines, including interleukin-1beta (IL-1beta) and tumor necrosis factor-alpha (TNF-alpha), have been correlated with the patients affected by ALD. However, the direct effect

Mutational spectrum induced by acetaldehyde in the HPRT gene of human T lymphocytes resembles that in the p53 gene of esophageal cancers.

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As the primary metabolite of alcohol, acetaldehyde (AA) may be responsible for many pathological effects related to consumption of alcohol, such as esophageal cancer. The spectrum of p53 mutations in esophageal tumors is indicative of the involvement of exogenous agents, such as tobacco smoke. There

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acetaldehyde/zhubný nádor

Benzo[a]pyrene, aflatoxine B₁ and acetaldehyde mutational patterns in TP53 gene using a functional assay: relevance to human cancer aetiology.

Short-term salivary acetaldehyde increase due to direct exposure to alcoholic beverages as an additional cancer risk factor beyond ethanol metabolism.

Reduction of oral acetaldehyde levels using a controlled-release chlorhexidine chip as a prevention strategy against upper digestive tract cancer.

Ethanol-induced oxidative stress and acetaldehyde formation in rat mammary tissue: potential factors involved in alcohol drinking promotion of breast cancer.

PPARalpha and PPARbeta are differentially affected by ethanol and the ethanol metabolite acetaldehyde in the MCF-7 breast cancer cell line.

Cancer induction in mice with acetaldehyde methylformylhydrazone of the false morel mushroom.

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

Evaluation of potential salivary acetaldehyde production from ethanol in oral cancer patients and healthy subjects.

Cytosolic xanthine oxidoreductase mediated bioactivation of ethanol to acetaldehyde and free radicals in rat breast tissue. Its potential role in alcohol-promoted mammary cancer.

Rat ventral prostate xanthine oxidase bioactivation of ethanol to acetaldehyde and 1-hydroxyethyl free radicals: analysis of its potential role in heavy alcohol drinking tumor-promoting effects.

Interrelationship between alcohol, smoking, acetaldehyde and cancer.

Genetic-epidemiological evidence for the role of acetaldehyde in cancers related to alcohol drinking.

Acetaldehyde burst protection of ADH1B*2 against alcoholism: an additional hormesis protection against esophageal cancers following alcohol consumption?

Acetaldehyde-induced interleukin-1beta and tumor necrosis factor-alpha production is inhibited by berberine through nuclear factor-kappaB signaling pathway in HepG2 cells.

Mutational spectrum induced by acetaldehyde in the HPRT gene of human T lymphocytes resembles that in the p53 gene of esophageal cancers.

Najkompletnejšia databáza liečivých bylín podporovaná vedou

Acetaldehyde burst protection of ADH1B2 against alcoholism: an additional hormesis protection against esophageal cancer*s following alcohol consumption?