Different mechanisms of arsenic related signaling in cellular proliferation, apoptosis and neo-plastic transformation

Medda, Nandita; De, Sujit Kumar; Maiti, Smarajit

doi:10.1016/j.ecoenv.2020.111752

Cited by 82 publications

(44 citation statements)

References 78 publications

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“…The high estimate of cell death in the untreated samples could be a result of extensive cell division, which increases the fluidity of the cell membrane and facilitates the penetration of PI. Inaccuracies in the assessment of cell death using the PI method have also been observed in previous studies [ 2 , 29 , 46 ].…”

Section: Resultssupporting

confidence: 71%

A Promising Method for the Determination of Cell Viability: The Membrane Potential Cell Viability Assay

Madorran

Stožer

Arsov

et al. 2022

Cells

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Determining the viability of cells is fraught with many uncertainties. It is often difficult to determine whether a cell is still alive, approaching the point of no return, or dead. Today, there are many methods for determining cell viability. Most rely on an indirect determination of cell death (metabolism, molecular transport, and leakage, to name a few). In contrast, we have developed a promising novel method for a “direct” determination of cell viability. The potential method assesses cell membrane integrity (which is essential for all viable cells) by measuring the electrical potential of the cell membrane. To test the assay, we chose two different cell types, blood macrophages (TLT) and breast cancer epithelial cells (MCF 7). We exposed them to seven different toxic scenarios (arsenic (V), UV light, hydrogen peroxide, nutrient starvation, Tetrabromobisphenol A, fatty acids, and 5-fluorouracil) to induce different cell death pathways. Under controlled test conditions, the assay showed good accuracy when comparing the toxicity assessment with well-established methods. Moreover, the method showed compatibility with live cell imaging. Although we know that further studies are needed to confirm the performance of the assay in other situations, the results obtained are promising for their wider application in the future.

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Section: Resultssupporting

confidence: 71%

A Promising Method for the Determination of Cell Viability: The Membrane Potential Cell Viability Assay

Madorran

Stožer

Arsov

et al. 2022

Cells

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“…DDB2 is involved in DNA damage repair of NER pathway in The occurrence of prostate cancer (Chen et al, 2017), malignant melanoma (Barckhausen et al, 2014), nasopharyngeal cancer (Wang et al, 2020), and many other tumors, which has been confirmed to regulate The tumor suppressor and transcription factor p53. In arsenic induced DNA damage, more and more scholars have confirmed that arsenic inhibits NER pathway by inhibiting p53 in recent years (Medda et al, 2021; Muenyi et al, 2011). In this study, Shen et al (Shen et al, 2008) exposed human colon cancer cells HCT116 with overexpression or deletion of p53 gene to arsenic, and confirmed that deletion of p53 expression can reduce p53 DNA binding activity.…”

Section: Discussionmentioning

confidence: 98%

Histone demethylase JHDM2A participates in the repair of arsenic-induced DNA damage in L-02 cells by regulating DDB2

Zhang²,

et al. 2022

Toxicol Ind Health

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Arsenic is widely present in nature and is a class I carcinogen confirmed by the World Health Organization and the International Agency for Research on Cancer. The liver is responsible for biotransformation in the body and is one of the major organs where arsenic accumulates in the body, but the mechanisms of arsenic-induced abnormal DNA damage repair pathways in the liver are still unclear. Recent studies have revealed that epigenetic mechanisms play an important role in arsenic-induced lesions. In this study, an in vitro model was established using human normal hepatocytes L-02 to investigate the mechanism of the specific demethylase JHDM2A of H3K9me2 in the repair of arsenic-induced DNA damage in L-02 cells. The results showed that with the increase of arsenic concentrations, the extent of DNA damage in L-02 cells showed an increasing trend and total intracellular H3K9me2 expression was downregulated. In addition, the enrichment level of H3K9me2 in the promoter region of DBB2, a key factor of nucleotide repair (NBR), increased, while protein and mRNA expression levels showed a decreasing trend. Thereafter, we overexpressed and repressed JHDM2A and found a close association between JHDM2A and arsenic-induced DNA damage. DDB2 protein and mRNA expression was downregulated with JHDM2A overexpression and upregulated with JHDM2A repression, while DBB2 promoter region H3K9me2 enrichment levels remained at a high level, although they were affected after JHDM2A overexpression or knockdown to some extent. These results suggest a potential mechanism by which JHDM2A may regulate DDB2 gene expression, participate in the NBR process, and play a role in arsenic-induced DNA damage in L-02 cells, which is not the result of JHDM2A exerting demethylation on H3K9me2 in the DDB2 promoter region. Our results provided an epigenetic mechanism for endemic arsenicosis, as well as a scientific basis for potential prevention and control measures.

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“…ROS is mainly derived from mitochondria, but can also in turn lead to mitochondrial stress, mitochondrial dysfunction, mitochondrial division, and cell apoptosis ( Medda et al, 2021 ). As noted above that the mitochondrial dysfunction can affect the energy supply and indirectly affect insulin secretion.…”

Section: The Generation and Damage Of Ros In T2dmentioning

confidence: 99%

Oxidative RNA Damage in the Pathogenesis and Treatment of Type 2 Diabetes

Chen

et al. 2022

Front. Physiol.

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Excessive production of free radicals can induce cellular damage, which is associated with many diseases. RNA is more susceptible to oxidative damage than DNA due to its single-stranded structure, and lack of protective proteins. Yet, oxidative damage to RNAs received little attention. Accumulating evidence reveals that oxidized RNAs may be dysfunctional and play fundamental role in the occurrence and development of type 2 diabetes (T2D) and its complications. Oxidized guanine nucleoside, 8-oxo-7, 8-dihydroguanine (8-oxoGuo) is a biomarker of RNA oxidation that could be associated with prognosis in patients with T2D. Nowadays, some clinical trials used antioxidants for the treatment of T2D, though the pharmacological effects remained unclear. In this review, we overview the cellular handling mechanisms and the consequences of the oxidative RNA damage for the better understanding of pathogenesis of T2D and may provide new insights to better therapeutic strategy.

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Different mechanisms of arsenic related signaling in cellular proliferation, apoptosis and neo-plastic transformation

Cited by 82 publications

References 78 publications

A Promising Method for the Determination of Cell Viability: The Membrane Potential Cell Viability Assay

A Promising Method for the Determination of Cell Viability: The Membrane Potential Cell Viability Assay

Histone demethylase JHDM2A participates in the repair of arsenic-induced DNA damage in L-02 cells by regulating DDB2

Oxidative RNA Damage in the Pathogenesis and Treatment of Type 2 Diabetes

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