NDLI: DNA Damage, Cell Cycle Arrest, and Apoptosis Induction Caused by Lead in Human Leukemia Cells

Content Provider	PubMed Central
Author	Yedjou, Clement G. Tchounwou, Hervey M. Tchounwou, Paul B.
Editor	Mielke, Howard W.
Copyright Year	2015
Abstract	In recent years, the industrial use of lead has been significantly reduced from paints and ceramic products, caulking, and pipe solder. Despite this progress, lead exposure continues to be a significant public health concern. The main goal of this research was to determine the in vitro mechanisms of lead nitrate [Pb(NO3)2] to induce DNA damage, apoptosis, and cell cycle arrest in human leukemia (HL-60) cells. To reach our goal, HL-60 cells were treated with different concentrations of Pb(NO3)2 for 24 h. Live cells and necrotic death cells were measured by the propidium idiode (PI) assay using the cellometer vision. Cell apoptosis was measured by the flow cytometry and DNA laddering. Cell cycle analysis was evaluated by the flow cytometry. The result of the PI demonstrated a significant (p < 0.05) increase of necrotic cell death in Pb(NO3)2-treated cells, indicative of membrane rupture by Pb(NO3)2 compared to the control. Data generated from the comet assay indicated a concentration-dependent increase in DNA damage, showing a significant increase (p < 0.05) in comet tail-length and percentages of DNA cleavage. Data generated from the flow cytometry assessment indicated that Pb(NO3)2 exposure significantly (p < 0.05) increased the proportion of caspase-3 positive cells (apoptotic cells) compared to the control. The flow cytometry assessment also indicated Pb(NO3)2 exposure caused cell cycle arrest at the G0/G1 checkpoint. The result of DNA laddering assay showed presence of DNA smear in the agarose gel with little presence of DNA fragments in the treated cells compared to the control. In summary, Pb(NO3)2 inhibits HL-60 cells proliferation by not only inducing DNA damage and cell cycle arrest at the G0/G1 checkpoint but also triggering the apoptosis through caspase-3 activation and nucleosomal DNA fragmentation accompanied by secondary necrosis. We believe that our study provides a new insight into the mechanisms of Pb(NO3)2 exposure and its associated adverse health effects.
Related Links	http://dx.doi.org/10.3390/ijerph13010056
Starting Page	56
File Format	PDF
ISSN	16604601
e-ISSN	16604601
Journal	International Journal of Environmental Research and Public Health
Issue Number	1
Volume Number	13
Language	English
Publisher	MDPI
Publisher Date	2015-12-01
Access Restriction	Open
Rights Holder	MDPI
Subject Keyword	Research in Higher Education
Content Type	Text
Resource Type	Article
Subject	Health, Toxicology and Mutagenesis Pollution Public Health, Environmental and Occupational Health

Sl.	Authority	Responsibilities	Communication Details
1	Ministry of Education (GoI), Department of Higher Education	Sanctioning Authority	https://www.education.gov.in/ict-initiatives
2	Indian Institute of Technology Kharagpur	Host Institute of the Project: The host institute of the project is responsible for providing infrastructure support and hosting the project	https://www.iitkgp.ac.in
3	National Digital Library of India Office, Indian Institute of Technology Kharagpur	The administrative and infrastructural headquarters of the project	Dr. B. Sutradhar bsutra@ndl.gov.in
4	Project PI / Joint PI	Principal Investigator and Joint Principal Investigators of the project	Dr. B. Sutradhar bsutra@ndl.gov.in Prof. Saswat Chakrabarti will be added soon
5	Website/Portal (Helpdesk)	Queries regarding NDLI and its services	support@ndl.gov.in
6	Contents and Copyright Issues	Queries related to content curation and copyright issues	content@ndl.gov.in
7	National Digital Library of India Club (NDLI Club)	Queries related to NDLI Club formation, support, user awareness program, seminar/symposium, collaboration, social media, promotion, and outreach	clubsupport@ndl.gov.in
8	Digital Preservation Centre (DPC)	Assistance with digitizing and archiving copyright-free printed books	dpc@ndl.gov.in
9	IDR Setup or Support	Queries related to establishment and support of Institutional Digital Repository (IDR) and IDR workshops	idr@ndl.gov.in

DNA Damage, Cell Cycle Arrest, and Apoptosis Induction Caused by Lead in Human Leukemia Cells

Avermectin induced DNA damage to the apoptosis and autophagy in human lung epithelial A549 cells

Induction of Cell Death, DNA Strand Breaks, and Cell Cycle Arrest in DU145 Human Prostate Carcinoma Cell Line by Benzo[a]pyrene and Benzo[a]pyrene-7,8-diol-9,10-epoxide

Cadmium Chloride Induces DNA Damage and Apoptosis of Human Liver Carcinoma Cells via Oxidative Stress

Induction of cell cycle arrest, DNA damage, and apoptosis by nimbolide in human renal cell carcinoma cells

Basic Apoptotic Mechanisms of Lead Toxicity in Human Leukemia (Hl-60) Cells

Silica nanoparticles cause spermatogenesis dysfunction in mice via inducing cell cycle arrest and apoptosis

The Influence of TRP53 in the Dose Response of Radiation-Induced Apoptosis, DNA Repair and Genomic Stability in Murine Haematopoietic Cells

DNA DAMAGE IN HUMAN SKIN KERATINOCYTES CAUSED BY MULTI-WALLED CARBON NANOTUBES WITH CARBOXYLATE FUNCTIONALIZATION

DNA Damage, Cell Cycle Arrest, and Apoptosis Induction Caused by Lead in Human Leukemia Cells

Similar Documents

DNA Damage, Cell Cycle Arrest, and Apoptosis Induction Caused by Lead in Human Leukemia Cells

Avermectin induced DNA damage to the apoptosis and autophagy in human lung epithelial A549 cells

Induction of Cell Death, DNA Strand Breaks, and Cell Cycle Arrest in DU145 Human Prostate Carcinoma Cell Line by Benzo[a]pyrene and Benzo[a]pyrene-7,8-diol-9,10-epoxide

Cadmium Chloride Induces DNA Damage and Apoptosis of Human Liver Carcinoma Cells via Oxidative Stress

Induction of cell cycle arrest, DNA damage, and apoptosis by nimbolide in human renal cell carcinoma cells

Basic Apoptotic Mechanisms of Lead Toxicity in Human Leukemia (Hl-60) Cells

Silica nanoparticles cause spermatogenesis dysfunction in mice via inducing cell cycle arrest and apoptosis

The Influence of TRP53 in the Dose Response of Radiation-Induced Apoptosis, DNA Repair and Genomic Stability in Murine Haematopoietic Cells

DNA DAMAGE IN HUMAN SKIN KERATINOCYTES CAUSED BY MULTI-WALLED CARBON NANOTUBES WITH CARBOXYLATE FUNCTIONALIZATION

DNA Damage, Cell Cycle Arrest, and Apoptosis Induction Caused by Lead in Human Leukemia Cells