Long term low-dose arsenic exposure induces loss of DNA methylation

Reichard, John F.; Schnekenburger, Michaël; Puga, Alvaro

doi:10.1016/j.bbrc.2006.11.001

Cited by 272 publications

(163 citation statements)

References 14 publications

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“…In contrast, more recent data from animal models have shown the possibility of a strong bond with liver tumor formation [261][262][263][264][265][266][267][268] . Various carcinogenic mechanisms, genetic and epigenetic, have been proposed: DNA methylation, oxidative damage, genomic instability and reduction of programmed cell death [269][270][271][272][273][274] .…”

Section: Arsenicmentioning

confidence: 99%

Hepatocellular carcinoma and the risk of occupational exposure

Rapisarda

Loreto

Malaguarnera

et al. 2016

WJH

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Hepatocellular carcinoma (HCC) is the most common type of liver cancer. The main risk factors for HCC are alcoholism, hepatitis B virus, hepatitis C virus, nonalcoholic steatohepatitis, obesity, type 2 diabetes, cirrhosis, aflatoxin, hemochromatosis, Wilson's disease and hemophilia. Occupational exposure to chemicals is another risk factor for HCC. Often the relationship between occupational risk and HCC is unclear and the reports are fragmented and inconsistent. This review aims to summarize the current knowledge regarding the association of infective and non-infective occupational risk exposure and HCC in order to encourage further research and draw attention to this global occupational public health problem. Core tip: Hepatocellular carcinoma (HCC) is the fifth most common human cancer. This review summarizes current knowledge regarding the occupational risk factors of HCC. In particular, we underline not only the infective but also non-infective occupational risk exposure, including chemical agents and toxic metabolites which are a major cause of liver damage.

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Section: Arsenicmentioning

confidence: 99%

Hepatocellular carcinoma and the risk of occupational exposure

Rapisarda

Loreto

Malaguarnera

et al. 2016

WJH

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“…In addition to its potent mutagenic action, arsenic can act through epigenetic mechanisms that modify DNA methylation patterns. The metal ion has been shown to deplete SAM and repress DNMT1 and DNMT3A [70]. Other metals, such as lead and nickel, have also been reported to have relevance in transplacental exposures and later carcinogenic effects by acting through epigenetic mechanisms [71,72].…”

Section: Heavy Metals-mentioning

confidence: 99%

Epigenetic reprogramming and imprinting in origins of disease

Tang

2007

Rev Endocr Metab Disord

217

134

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The traditional view that gene and environment interactions control disease susceptibility can now be expanded to include epigenetic reprogramming as a key determinant of origins of human disease. Currently, epigenetics is defined as heritable changes in gene expression that do not alter DNA sequence but are mitotically and trans-generationally inheritable. Epigenetic reprogramming is the process by which an organism's genotype interacts with the environment to produce its phenotype and provides a framework for explaining individual variations and the uniqueness of cells, tissues, or organs despite identical genetic information. The main epigenetic mediators are histone modification, DNA methylation, and non-coding RNAs. They regulate crucial cellular functions such as genome stability, X-chromosome inactivation, gene imprinting, and reprogramming of non-imprinting genes, and work on developmental plasticity such that exposures to endogenous or exogenous factors during critical periods permanently alter the structure or function of specific organ systems. Developmental epigenetics is believed to establish "adaptive" phenotypes to meet the demands of the later-life environment. Resulting phenotypes that match predicted later-life demands will promote health, while a high degree of mismatch will impede adaptability to later-life challenges and elevate disease risk. The rapid introduction of synthetic chemicals, medical interventions, environmental pollutants, and lifestyle choices, may result in conflict with the programmed adaptive changes made during early development, and explain the alarming increases in some diseases. The recent identification of a significant number of epigenetically regulated genes in various model systems has prepared the field to take on the challenge of characterizing distinct epigenomes related to various diseases. Improvements in human health could then be redirected from curative care to personalized, preventive medicine based, in part, on epigenetic markings etched in the "margins" of one's genetic make-up. NIH Public Access Author ManuscriptRev Endocr Metab Disord. Author manuscript; available in PMC 2014 June 13. Epigenetics meets genetics in disease susceptibilityIn the past, susceptibility of disease was believed to be determined solely by inheritable information carried on the primary sequence of the DNA. Individuals are endowed with different genotypes that dictate how they respond to endogenous factors such as development cues, hormones, and cytokines or to exogenous influences, including nutrient availability, infection, physical activities, social behavior, and other environmental factors. Over time, these responses form the basis of genetic variability to disease susceptibility. Aberrant changes in linear DNA sequence result in mutations, deletions, gene fusion, tandem duplications, or gene amplifications causing dysregulation of gene expression that underlies the genesis of disease [1][2][3][4][5][6][7]. Recently, however, it has become clear that epigenetic disr...

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“…In humans, DNA methylation is initiated by the de novo DNA methyltransferase 3 (DNMT3A and B) and maintained by DNA methyltransferase 1 (DNMT1) (39). Following low-dose iAs exposure, the expression of the DNMTs is reduced, which results in less methylation at target sites (40)(41)(42). Because DNMTs also participate in DNA repair, inactivation and/or reduction in the expression levels of DNA methyltransferases will also impede DNA repair efficiency (35,41,43,44).…”

Section: Dna Methylationmentioning

confidence: 99%

Epigenomic reprogramming in inorganic arsenic-mediated gene expression patterns during carcinogenesis

Eckstein

Eleazer

Rea

et al. 2017

Reviews on Environmental Health

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Abstract Arsenic is a ubiquitous metalloid that is not mutagenic but is carcinogenic. The mechanism(s) by which arsenic causes cancer remain unknown. To date, several mechanisms have been proposed, including the arsenic-induced generation of reactive oxygen species (ROS). However, it is also becoming evident that inorganic arsenic (iAs) may exert its carcinogenic effects by changing the epigenome, and thereby modifying chromatin structure and dynamics. These epigenetic changes alter the accessibility of gene regulatory factors to DNA, resulting in specific changes in gene expression both at the levels of transcription initiation and gene splicing. In this review, we discuss recent literature reports describing epigenetic changes induced by iAs exposure and the possible epigenetic mechanisms underlying these changes.

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Long term low-dose arsenic exposure induces loss of DNA methylation

Cited by 272 publications

References 14 publications

Hepatocellular carcinoma and the risk of occupational exposure

Hepatocellular carcinoma and the risk of occupational exposure

Epigenetic reprogramming and imprinting in origins of disease

Epigenomic reprogramming in inorganic arsenic-mediated gene expression patterns during carcinogenesis

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