Association of H3K79 monomethylation (an epigenetic signature) with arsenic-induced skin lesions

Bhattacharjee, Pritha; Paul, Somnath; Bhattacharjee, Sandip; Giri, Ashok K.

doi:10.1016/j.mrfmmm.2017.11.001

Cited by 20 publications

(8 citation statements)

References 89 publications

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“…The West Bengal population (30 million people) are exposed to arsenic through ground water and 15-20% of the individuals have arsenicosis (dermatological anomalies) [307]. Epigenetic analyses of peripheral blood mononuclear cells (PBMC) suggest that the DNA repair system is defective in the exposed population (urinary arsenic up to 434.1 µg/L compared to control with concentrations up to 33.7 µg/L) with arsenicosis symptoms [308].…”

Section: Dna Repairmentioning

confidence: 99%

Integration of Epigenetic Mechanisms into Non-Genotoxic Carcinogenicity Hazard Assessment: Focus on DNA Methylation and Histone Modifications

Desaulniers

Vasseur

Jacobs

et al. 2021

IJMS

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Epigenetics involves a series of mechanisms that entail histone and DNA covalent modifications and non-coding RNAs, and that collectively contribute to programing cell functions and differentiation. Epigenetic anomalies and DNA mutations are co-drivers of cellular dysfunctions, including carcinogenesis. Alterations of the epigenetic system occur in cancers whether the initial carcinogenic events are from genotoxic (GTxC) or non-genotoxic (NGTxC) carcinogens. NGTxC are not inherently DNA reactive, they do not have a unifying mode of action and as yet there are no regulatory test guidelines addressing mechanisms of NGTxC. To fil this gap, the Test Guideline Programme of the Organisation for Economic Cooperation and Development is developing a framework for an integrated approach for the testing and assessment (IATA) of NGTxC and is considering assays that address key events of cancer hallmarks. Here, with the intent of better understanding the applicability of epigenetic assays in chemical carcinogenicity assessment, we focus on DNA methylation and histone modifications and review: (1) epigenetic mechanisms contributing to carcinogenesis, (2) epigenetic mechanisms altered following exposure to arsenic, nickel, or phenobarbital in order to identify common carcinogen-specific mechanisms, (3) characteristics of a series of epigenetic assay types, and (4) epigenetic assay validation needs in the context of chemical hazard assessment. As a key component of numerous NGTxC mechanisms of action, epigenetic assays included in IATA assay combinations can contribute to improved chemical carcinogen identification for the better protection of public health.

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Section: Dna Repairmentioning

confidence: 99%

Integration of Epigenetic Mechanisms into Non-Genotoxic Carcinogenicity Hazard Assessment: Focus on DNA Methylation and Histone Modifications

Desaulniers

Vasseur

Jacobs

et al. 2021

IJMS

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“…Furthermore, different social stigma, superstitions, and prejudices about the skin symptoms further worsen the situation. In our own studies ( 38 , 93 , 116 ), while performing random sampling in such affected areas, we have faced discontent and discomfort among individuals and family members to acknowledge the fact of skin lesions like skin darkening, black spots, nodules, gangrene, and cancer in limbs, which causes social isolation of the victims. This stigma makes it difficult for our onboard dermatologists to determine whether an individual's dermatological lesion is due to arsenic or something else.…”

Section: Discussionmentioning

confidence: 99%

“…However, none of the studies particularly differentiate the degree of altered PTHM between arsenic-exposed skin lesion phenotypes compared to those with no skin lesion. Recently, our group has reported about two different PTHMs among chronic arsenic-exposed population from India considering the skin lesion status ( 38 , 116 ). We identified significant upregulation of H3K79me1 in individuals with arsenic-induced skin lesion, and H3K79me1 was found to be regulated by the upstream methyltransferase DOT1L.…”

Section: Understanding the Present State Of Researchmentioning

confidence: 99%

Recent Advances in Arsenic Research: Significance of Differential Susceptibility and Sustainable Strategies for Mitigation

Sanyal

Bhattacharjee

Paul

2020

Front. Public Health

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Arsenic contamination in drinking water and associated adverse outcomes are one of the major health issues in more than 50 countries worldwide. The scenario is getting even more detrimental with increasing number of affected people and newer sites reported from all over the world. Apart from drinking water, the presence of arsenic has been found in various other dietary sources. Chronic arsenic toxicity affects multiple physiological systems and may cause malignancies leading to death. Exposed individuals, residing in the same area, developed differential dermatological lesion phenotypes and varied susceptibility toward various other arsenic-induced disease risk, even after consuming equivalent amount of arsenic from the similar source, over the same duration of time. Researches so far indicate that differential susceptibility plays an important role in arsenic-induced disease manifestation. In this comprehensive review, we have identified major population-based studies of the last 20 years, indicating possible causes of differential susceptibility emphasizing arsenic methylation capacity, variation in host genome (single nucleotide polymorphism), and individual epigenetic pattern (DNA methylation, histone modification, and miRNA expression). Holistic multidisciplinary strategies need to be implemented with few sustainable yet cost-effective solutions like alternative water source, treatment of arsenic-contaminated water, new adaptations in irrigation system, simple modifications in cooking strategy, and dietary supplementations to combat this menace. Our review focuses on the present perspectives of arsenic research with special emphasis on the probable causes of differential susceptibility toward chronic arsenic toxicity and sustainable remediation strategies.

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“…The mechanism underlying arsenic L1 induction is not known; however, numerous studies (Paul et al ., ) found a significant arsenic‐induced L1 hypomethylation. It has been observed that the presence of arsenic leads to a decreased availability of SAM pool within the cell and to a drop in the total methylation index of the genome as well as the histones (Paul and Giri, ); (Bhattacharjee et al ., )). Therefore, it has been suggested that epigenetic alteration can be the most important mechanism causing L1 induction, and that L1 methylation could be considered as a potent epigenetic signature for arsenic toxicity (Paul et al ., ).…”

Section: Environmental Chemical Agents and Their Effect On L1‐rtpmentioning

confidence: 99%

Long INterspersed element‐1 mobility as a sensor of environmental stresses

Giorgi

2020

Environ and Mol Mutagen

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Long INterspersed element (LINE-1, L1) retrotransposons are the most abundant transposable elements in the human genome, constituting approximately 17%. They move by a "copy-paste" mechanism, involving reverse transcription of an RNA intermediate and insertion of its cDNA copy at a new site in the genome. L1 retrotransposition (L1-RTP) can cause insertional mutations, alter gene expression, transduce exons, and induce epigenetic dysregulation. L1-RTP is generally repressed; however, a number of observations collected over about 15 years revealed that it can occur in response to environmental stresses. Moreover, emerging evidence indicates that L1-RTP can play a role in the onset of several neurological and oncological diseases in humans. In recent years, great attention has been paid to the exposome paradigm, which proposes that health effects of an environmental factor should be evaluated considering both cumulative environmental exposures and the endogenous processes resulting from the biological response. L1-RTP could be an endogenous process considered for this application. Here, we summarize the current understanding of environmental factors that can affect the retrotransposition of human L1 elements. Evidence indicates that L1-RTP alteration is triggered by numerous and various environmental stressors, such as chemical agents (heavy metals, carcinogens, oxidants, and drugs), physical agents (ionizing and non-ionizing radiations), and experiential factors (voluntary exercise, social isolation, maternal care, and environmental light/dark cycles). These data come from in vitro studies on cell lines and in vivo studies on transgenic animals: future investigations should be focused on physiologically relevant models to gain a better understanding of this topic.

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Association of H3K79 monomethylation (an epigenetic signature) with arsenic-induced skin lesions

Cited by 20 publications

References 89 publications

Integration of Epigenetic Mechanisms into Non-Genotoxic Carcinogenicity Hazard Assessment: Focus on DNA Methylation and Histone Modifications

Integration of Epigenetic Mechanisms into Non-Genotoxic Carcinogenicity Hazard Assessment: Focus on DNA Methylation and Histone Modifications

Recent Advances in Arsenic Research: Significance of Differential Susceptibility and Sustainable Strategies for Mitigation

Long INterspersed element‐1 mobility as a sensor of environmental stresses

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