Effect of arsenic on DNA damage, glutathione content, apoptosis and necrosis in HaCat cells

Toxicology ◽  
2007 ◽  
Vol 231 (2-3) ◽  
pp. 116-117 ◽  
Author(s):  
G BENHUSEIN ◽  
E MUTCH ◽  
F WILLIAMS
Keyword(s):  
Dna Damage ◽  
Hacat Cells ◽  
Apoptosis And Necrosis

scholarly journals Deleterious effect of mercuric chloride on human epithelial cells

2021 ◽  
Author(s):  
Changhai (Kevin) Ji
Keyword(s):  
Dna Damage ◽  
Cell Death ◽  
Epithelial Cells ◽  
Human Health ◽  
Exposure Time ◽  
Mercuric Chloride ◽  
Deleterious Effect ◽  
Detection Techniques ◽  
Human Epithelial Cells ◽  
Apoptosis And Necrosis

This thesis studied the cytotoxicity of mercuric chloride on human epihelial cells. The three detection techniques were developed to monitor the cytotoxicity of soluble mercuric chloride to human health. Both increased concentration and exposure time resulted in increased DNA damage and cell death. At lower levels death occurred by a mixture of apoptosis and necrosis, while at higher levels cell death occurred primarily by necrosis. This is the first study to demonstrate a deleterious effect of soluble mercuric chloride on human epithelial cells, although mercury has long been known as nephrotoxic and neurotoxic.

scholarly journals Genotoxic Effect of Arsenate and Arsenite in Human HaCat Cells in Culture Using Comet Assay

2020 ◽  
pp. 36-44
Author(s):  
Ghazalla Benhusein ◽  
Elaine Mutch ◽  
Faith M. Williams
Keyword(s):  
Dna Damage ◽  
Comet Assay ◽  
Statistical Significance ◽  
Human Keratinocytes ◽  
Hacat Cells ◽  
Environmental Chemical ◽  
Viable Cells ◽  
Buthionine Sulphoximine ◽  
Ros Formation

Arsenic is an environmental chemical of toxicological concern today since it is a human genotoxin and chronic exposure is associated with development of cancers, including skin. Inorganic arsenate is metabolically reduced to arsenite by glutathione (GSH) prior to methylation. The aim of this study was to determine the relative toxic effects of arsenate and arsenite in HaCat cells (immortalized human keratinocytes) in vitro by measuring cytotoxicity, DNA damage, depletion of glutathione and apoptotic and necrotic events. HaCat cells were treated with arsenate and arsenite (10 μM) for DNA damage detection using Comet assay and cytotoxicity (10, 60 and 100 μM) all measured at 24 hr. In some experiment arsenate or arsenite (10 μM) was added at the same time as BSO 10 μM for 24 hr, and GSH levels were measured by HPLC with fluorescence detection. Flow cytometry was used to investigate apoptotic and necrotic events following arsenate and arsenite (10 μM) treatment for 24 hr. Arsenate and arsenite at 60 and 100 μM, but not 10 μM, reduced the number of adherent viable cells with time. Therefore, DNA damage could only be measured at 10 μM as at higher concentrations the cells did not produce classical Comets but showed fragmentation. DNA damage was significantly (p < 0.001) increased in cells treated for 24 hr with 10 μM arsenate and arsenite compared to control. GSH levels were significantly increased in HaCat cells treated with10 μM arsenate and arsenite (p < 0.05, p < 0.001, respectively) compared to control. Cells treated with buthionine sulphoximine (BSO) at the same time as arsenate had increased GSH levels (p < 0.001), but arsenite and BSO did not increase cellular GSH. Arsenate and arsenite increased apoptosis, and arsenate increased necrosis, although none of the values reached statistical significance. Arsenite was more cytotoxic than arsenate. Arsenate and arsenite are known to produce oxidative stress involving ROS formation and depletion of glutathione. The increase in GSH levels at low doses of arsenate and arsenite, and by arsenate even in the presence of BSO.

In vitro assessment of anticytotoxic and antigenotoxic effects of CANOVA®

Homeopathy ◽  
2016 ◽  
Vol 105 (03) ◽  
pp. 265-269 ◽  
Author(s):  
Henrique Fonseca Sousa do Nascimento ◽  
Plínio Cerqueira dos Santos Cardoso ◽  
Helem Ferreira Ribeiro ◽  
Tatiane Cristina Mota ◽  
Lorena Monteiro Gomes ◽  
...  
Keyword(s):  
Dna Damage ◽  
Human Lymphocytes ◽  
Nitroso Compound ◽  
Cytoprotective Effect ◽  
In Vitro Assessment ◽  
Induced Apoptosis ◽  
Clinical Conditions ◽  
Apoptosis And Necrosis ◽  
Antigenotoxic Effects

Background: CANOVA® (CA) is a homeopathic immunomodulator. It contains several homeopathic medicines prepares according to the Brazilian Pharmacopoeia. CA is indicated in clinical conditions in which the immune system is impaired and against tumors. N-methyl-N-nitrosourea (NMU) is an N-nitroso compound, with genotoxic/mutagenic properties. Although several studies have shown promising results in the use of CA, there are no studies reporting possible antigenotoxic effects. Method: This study evaluated the in vitro antigenotoxic and anticytotoxic effects of CA in human lymphocytes exposed to NMU. Samples of human lymphocytes that were subjected to different concentrations of a mixture containing CA and NMU were used. The genotoxicity/antigenotoxicity of CA was evaluated by the comet assay, anticytotoxicity was assessed by quantification of apoptosis and necrosis using acridine orange/ethidium bromide. Results: CA significantly reduced DNA damage induced by NMU and reduced significantly the frequency of NMU-induced apoptosis after 24 h of treatment. Conclusion: CA has an important cytoprotective effect significantly reducing the DNA damage and apoptosis induced by the carcinogen NMU.

scholarly journals 513 Role of regnase1 in UVA-induced oxidative DNA damage and apoptosis in HaCaT cells

2016 ◽  
Vol 136 (9) ◽  
pp. S248
Author(s):  
A. Wolnicka-Glubisz ◽  
M. Smejda ◽  
A. Cierniak ◽  
A. Adamczyk ◽  
P. Konieczny
Keyword(s):  
Dna Damage ◽  
Oxidative Dna Damage ◽  
Hacat Cells

Capillary electrophoresis of DNA damage after irradiation: apoptosis and necrosis

2000 ◽  
Vol 871 (1-2) ◽  
pp. 321-330 ◽  
Author(s):  
Marı́a Teresa Valenzuela ◽  
Marı́a Isabel Núñez ◽  
Marı́a Rosario Guerrero ◽  
Mercedes Villalobos ◽  
José Mariano Ruiz de Almodóvar
Keyword(s):  
Dna Damage ◽  
Capillary Electrophoresis ◽  
Apoptosis And Necrosis

Role of H3K18ac-regulated nucleotide excision repair-related genes in arsenic-induced DNA damage and repair of HaCaT cells

2020 ◽  
Vol 39 (9) ◽  
pp. 1168-1177 ◽  
Author(s):  
AL Zhang ◽  
L Chen ◽  
L Ma ◽  
XJ Ding ◽  
SF Tang ◽  
...  
Keyword(s):  
Dna Damage ◽  
Nucleotide Excision Repair ◽  
Molecular Mechanisms ◽  
Excision Repair ◽  
The Body ◽  
Hacat Cells ◽  
Transcriptional Expression ◽  
Promoter Regions ◽  
Nucleotide Excision

Arsenic is an environmental poison and is a grade I human carcinogen that can cause many types of damage to the body. The skin is one of the main target organs of arsenic damage, but the molecular mechanisms underlying arsenic poisoning are not clear. Arsenic is an epigenetic agent. Histone acetylation is one of the earliest covalent modifications to be discovered and is closely related to the occurrence and development of tumors. To investigate the role of acetylated histone H3K18 (H3K18 ac) in arsenic-induced DNA damage, HaCaT cells were exposed to sodium arsenite (NaAsO2) for 24 h. It was found that arsenic induced the downregulation of xeroderma pigmentosum A, D, and F ( XPA, XPD, and XPF—nucleotide excision repair (NER)-related genes) expression, as well as histone H3K18 ac expression, and aggravated DNA damage. Chromatin immunoprecipitation quantitative polymerase chain reaction (ChIP-qPCR) analysis showed that H3K18 acetylation in the promoter regions of XPA, XPD, and XPF was downregulated. In addition, the use of the histone deacetylase inhibitor trichostatin A (TSA) partially inhibited arsenic-induced DNA damage, inhibited deacetylation of H3K18 ac in the promoter regions of XPA, XPD, and XPF genes, increased acetylation of H3K18, and promoted the transcriptional expression of NER-related genes. Our study revealed that NaAsO2 induces DNA damage and inhibits the expression of NER-related genes, while TSA increases the H3K18 ac enrichment level and promotes the transcriptional expression of NER, thereby inhibiting DNA damage. These findings provide new ideas for understanding the molecular mechanisms underlying arsenic-induced skin damage.

DNA damage in lead-exposed hepatocytes: coexistence of apoptosis and necrosis?

2011 ◽  
Vol 35 (2) ◽  
pp. 208-217 ◽  
Author(s):  
Kilarkaje Narayana ◽  
Raj Raghupathy
Keyword(s):  
Dna Damage ◽  
Apoptosis And Necrosis
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