Arsenic-Induced Mutagenesis and Carcinogenesis

Maiti, Smarajit

doi:10.1016/b978-0-12-418688-0.00009-5

Cited by 4 publications

(1 citation statement)

References 275 publications

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“…Arsenic-induced skin lesions are characteristic by veracious hyperkeratosis and pigmentation disorders [ 10 ]. Other skin lesions associated with human arsenic exposure involves Bowen’s disease and squamous cell or basal cell carcinoma [ 11 – 14 ]. Sarkar et al showed that arsenic may exert toxicity via oxidative stress, indicated by related metabolic biomarkers [ 15 ].…”

Section: Introductionmentioning

confidence: 99%

Integration of microRNAome, proteomics and metabolomics to analyze arsenic-induced malignant cell transformation

Zhou

Yan

et al. 2017

Oncotarget

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Long-term exposure to arsenic has been linked to tumorigenesis in different organs and tissues, such as skin; however, the detailed mechanism remains unclear. In this present study, we integrated "omics" including microRNAome, proteomics and metabolomics to investigate the potential molecular mechanisms. Compared with non-malignant human keratinocytes (HaCaT), twenty-six miRNAs were significantly altered in arsenic-induced transformed cells. Among these miRNAs, the differential expression of six miRNAs was confirmed using Q-RT-PCR, representing potential oxidative stress genes. Two-dimensional gel electrophoresis (2D-PAGE) and mass spectrometry (MS) were performed to identify the differential expression of proteins in arsenic-induced transformed cells, and twelve proteins were significantly changed. Several proteins were associated with oxidative stress and carcinogenesis including heat shock protein beta-1 (HSPB1), peroxiredoxin-2 (PRDX2). Using ultraperformance liquid chromatography and Q-TOF mass spectrometry (UPLC/Q-TOF MS), 68 metabolites including glutathione, fumaric acid, citric acid, phenylalanine, and tyrosine, related to redox metabolism, glutathione metabolism, citrate cycle, met cycle, phenylalanine and tyrosine metabolism were identified and quantified. Taken together, these results indicated that arsenic-induced transformed cells exhibit alterations in miRNA, protein and metabolite profiles providing novel insights into arsenic-induced cell malignant transformation and identifying early potential biomarkers for cutaneous squamous cell carcinoma induced by arsenic.

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Section: Introductionmentioning

confidence: 99%

Integration of microRNAome, proteomics and metabolomics to analyze arsenic-induced malignant cell transformation

Zhou

Yan

et al. 2017

Oncotarget

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Understanding arsenic toxicity: Implications for environmental exposure and human health

kaur,

Garkal,

Sarode

et al. 2024

Journal of Hazardous Materials Letters

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Insights into the mechanisms of arsenic-selenium interactions and the associated toxicity in plants, animals, and humans: A critical review

Ali

Zhang

Junaid

et al. 2020

Critical Reviews in Environmental Science and Technology

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Arsenic (As) is toxic for humans, animals, and plants, whereas selenium (Se) is considered as an essential trace element and can cause toxicity during episodic elevated exposure.Interaction between As and Se is a critical factor for a detailed systematic understanding of the transportation, environmental fate, and associated toxicological effects of these metalloids in biological systems. Arsenic and Se induce cytotoxicity and genotoxicity through the generation of reactive oxidation species (ROS). Compared to arsenite (As III ), the methylated arsenicals, including methylarsonous acid (MAs III ) and dimethylarsinous acids (DMAs III ) exhibit more cytotoxic and genotoxic potentials to inhibit more potent enzymes and activate AP˗1 protein, which is a critical marker for genetic stability.Methylated As III and associated metabolites are well-known potential carcinogens that induce toxicity by blocking Se metabolism pathway. Low concentrations of Se compounds under reducing conditions inhibit the DNA repairing process and constraint the binding of zinc finger protein to DNA and ultimately cause the release of zinc from the motif of the zinc finger. Imbalance of Se compounds can lead to the generation of ROS, which can inhibit or decrease genomic stability. Arsenic and Se nexus also affect cellular signaling through activation of the transcription factors such as NFҡB and AP-1. In a nutshell, this review highlights As and Se sources in the environment, their uptake in soil-plant system, interactions between these metals and associated toxicity in major biological compartments, which may assist in addressing the hazardous impacts associated with As and Se contamination. Last but not the lease, this review also summarizes the available remedial measures and future research directions to cope with this critical issue.

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Arsenic-Induced Mutagenesis and Carcinogenesis

Cited by 4 publications

References 275 publications

Integration of microRNAome, proteomics and metabolomics to analyze arsenic-induced malignant cell transformation

Integration of microRNAome, proteomics and metabolomics to analyze arsenic-induced malignant cell transformation

Understanding arsenic toxicity: Implications for environmental exposure and human health

Insights into the mechanisms of arsenic-selenium interactions and the associated toxicity in plants, animals, and humans: A critical review

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