scholarly journals Use of the Tail Moment of the Lymphocytes to Evaluate DNA Damage in Human Biomonitoring Studies

2004 ◽  
Vol 81 (1) ◽  
pp. 121-132 ◽  
Author(s):  
E. Lee
Keyword(s):  
Dna Damage ◽  
Human Biomonitoring ◽  
Tail Moment

scholarly journals SMOKING GENOTOXICITY IN PERIPHERAL BLOOD LYMPHOCYTES USING THE COMET ASSAY

2013 ◽  
Vol 03 (03) ◽  
pp. 038-041
Author(s):  
Shobha S. Shetty ◽  
Hrishikesh Nachane
Keyword(s):  
Dna Damage ◽  
Comet Assay ◽  
Peripheral Blood ◽  
Peripheral Blood Lymphocytes ◽  
The Body ◽  
P Value ◽  
Tail Moment ◽  
Blood Lymphocytes ◽  
Significant Difference ◽  
Almost All

Abstract Background: Smoking has been shown to have a positive effect on DNA damage in almost all the cells of the body. Quantitative analysis of this damage will help in assessing the etiopathogenesis of various nicotine induced damage to the body. Comet assay has been an emerging tool in this regard and hence was applied by us to estimate the severity of DNA damage in smokers. Aims & Objectives: To evaluate the DNA genotoxicity in peripheral blood lymphocytes in smokers and their comparison with non smokers & assess the quantitative damage. Materials and methods: 30 smokers & 20 non smokers were recruited & their peripheral blood was taken for the comet assay to look for Olive moment & Tail moment to quantitatively assess the DNA damage due to cigarette smoking. Results: In our study there was no significant difference in the analysis of DNA damage (with regard to tail moment & olive moment) in smokers versus non smokers (P value: more than 0.05). Conclusions: Though smoking is known to cause DNA damage, we did not find significant differences between the two groups probably due to other multifactorial etiologies for genotoxicity.

scholarly journals Bone Marrow Oxidative Stress and Acquired Lineage-Specific Genotoxicity in Hematopoietic Stem/Progenitor Cells Exposed to 1,4-Benzoquinone

2020 ◽  
Vol 17 (16) ◽  
pp. 5865
Author(s):  
Ramya Dewi Mathialagan ◽  
Zariyantey Abd Hamid ◽  
Qing Min Ng ◽  
Nor Fadilah Rajab ◽  
Salwati Shuib ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Bone Marrow ◽  
Dna Damage ◽  
Progenitor Cells ◽  
Bone Marrow Cells ◽  
Protein Carbonyls ◽  
Mouse Bone Marrow ◽  
Tail Moment ◽  
Erythroid Progenitor ◽  
Hematopoietic Stem

Hematopoietic stem/progenitor cells (HSPCs) are susceptible to benzene-induced genotoxicity. However, little is known about the mechanism of DNA damage response affecting lineage-committed progenitors for myeloid, erythroid, and lymphoid. Here, we investigated the genotoxicity of a benzene metabolite, 1,4-benzoquinone (1,4-BQ), in HSPCs using oxidative stress and lineage-directed approaches. Mouse bone marrow cells (BMCs) were exposed to 1,4-BQ (1.25–12 μM) for 24 h, followed by oxidative stress and genotoxicity assessments. Then, the genotoxicity of 1,4-BQ in lineage-committed progenitors was evaluated using colony forming cell assay following 7–14 days of culture. 1,4-BQ exposure causes significant decreases (p < 0.05) in glutathione level and superoxide dismutase activity, along with significant increases (p < 0.05) in levels of malondialdehyde and protein carbonyls. 1,4-BQ exposure induces DNA damage in BMCs by significantly (p < 0.05) increased percentages of DNA in tail at 7 and 12 μM and tail moment at 12 μM. We found crucial differences in genotoxic susceptibility based on percentages of DNA in tail between lineage-committed progenitors. Myeloid and pre-B lymphoid progenitors appeared to acquire significant DNA damage as compared with the control starting from a low concentration of 1,4-BQ exposure (2.5 µM). In contrast, the erythroid progenitor showed significant damage as compared with the control starting at 5 µM 1,4-BQ. Meanwhile, a significant (p < 0.05) increase in tail moment was only notable at 7 µM and 12 µM 1,4-BQ exposure for all progenitors. Benzene could mediate hematological disorders by promoting bone marrow oxidative stress and lineage-specific genotoxicity targeting HSPCs.

scholarly journals THE BIOCHEMICAL ALTERATION AND DNA DAMAGE IN RATS (RATTUS RATTUS) AFTER CHRONIC INTRAPERITONEALLY INJECTION TO PURIFIED MICROCYSTIN-LR FROM ANABAENA CIRCINALIS

2017 ◽  
Vol 10 (11) ◽  
pp. 277
Author(s):  
Maher M Khadairi ◽  
Moayed Jy Al-amari ◽  
Ayad Mj Al-mamoori
Keyword(s):  
Dna Damage ◽  
Gel Electrophoresis ◽  
Biochemical Markers ◽  
Chronic Exposure ◽  
High Performance ◽  
Rattus Rattus ◽  
Tail Length ◽  
Oxygen Species ◽  
Tail Moment ◽  
Single Cell Gel Electrophoresis

  Objective: This study determined the effect of purified microcystin-leucine arginine (MC-LR) on biochemical and DNA damage parameters in rats.Methods: Utilization of preparative high-performance liquid chromatography in analysis, purification and collection of MC-LR, then intraperitoneally injection of purified MC-LR to rats. At the end of exposure, animals were sacrificed, and liver cell was isolated to measure the biochemical markers such as superoxide dismutase (SOD), catalase (CAT) and glutathione (GSH) as well as measured malondialdehyde (MDA), reactive oxygen species (ROS) and cytochrome P450 (Cyt P450), and DNA damage markers such as comet length, tail length, and tail moment were measured with the single cell gel electrophoresis also called comet assay.Results: The present results showed significantly increased activities of SOD as well as concentration of MDA, ROS with increasing concentration of MC-LR but the activities of CAT and GSH, as well as Cyt P450, were significantly decreased with increasing MC-LR dose while makers of DNA damage such as comet length, tail length, and tail moment also significantly increased with increasing MC-LR dose.Conclusion: This study demonstrated that chronic exposure to MC-LR toxin can induce alteration of biochemical and DNA damage markers.

scholarly journals Inhibition of AKT-Signaling Sensitizes Soft Tissue Sarcomas (STS) and Gastrointestinal Stromal Tumors (GIST) to Doxorubicin via Targeting of Homology-Mediated DNA Repair

2020 ◽  
Vol 21 (22) ◽  
pp. 8842
Author(s):  
Sergei Boichuk ◽  
Firuza Bikinieva ◽  
Ilmira Nurgatina ◽  
Pavel Dunaev ◽  
Elena Valeeva ◽  
...  
Keyword(s):  
Dna Damage ◽  
Dna Repair ◽  
Soft Tissue ◽  
Gastrointestinal Stromal Tumors ◽  
Topoisomerase Ii ◽  
Soft Tissue Sarcomas ◽  
Akt Signaling ◽  
Chemotherapeutic Agents ◽  
Tail Moment ◽  
Stromal Tumors

Activation of the phosphoinositide 3-kinase (PI3K)/Akt/mTOR pathway is well documented for a broad spectrum of human malignancies supporting their growth and progression. Accumulating evidence has also implicated AKT as a potent modulator of anti-cancer therapies via regulation of DNA damage response and repair (DDR) induced by certain chemotherapeutic agents and ionizing radiation (IR). In the present study, we examined the role of AKT signaling in regulating of Rad51 turnover and cytotoxic effects of topoisomerase II inhibitor, doxorubicin (Dox) in soft tissue sarcomas (STS) and gastrointestinal stromal tumors (GIST) in vitro. Blocking of AKT signaling (MK-2206) enhanced cytotoxic and pro-apoptotic effects of Dox in vast majority of STS and GIST cell lines. The phosphorylated form of Akt co-immunoprecipitates with Rad51 after Dox-induced DNA damage, whereas Akt inhibition interrupts this interaction and decreases Rad51 protein level by enhancing protein instability via proteasome-dependent degradation. Inhibition of Akt signaling in Dox-treated cells was associated with the increased number of γ-H2AX-positive cells, decrease of Rad51 foci formation and its colocalization with γ-H2AX foci, thereby revealing unsuccessful DDR events. This was also in consistency with an increase of tail moment (TM) and olive tail moment (OTM) in Dox-treated GIST and STS cells cultured in presence of Akt inhibitor after Dox washout. Altogether, our data illustrates that inhibition of AKT signaling is STS and GIST might potentiate the cytotoxic effect of topoisomerase II inhibitors via attenuating the homology-mediated DNA repair.

DNA effects of low level occupational exposure to extremely low frequency electromagnetic fields (50/60 Hz)

2019 ◽  
Vol 35 (6) ◽  
pp. 424-430 ◽  
Author(s):  
Rezvan Zendehdel ◽  
Il Je Yu ◽  
Behnam Hajipour-Verdom ◽  
Zahra Panjali
Keyword(s):  
Dna Damage ◽  
Occupational Exposure ◽  
Low Frequency ◽  
International Agency ◽  
Tail Moment ◽  
Limit Values ◽  
Strand Breaks ◽  
Extremely Low Frequency ◽  
Exposed Population ◽  
Exposure Levels

Aims: Exposure to extremely low frequency magnetic fields (ELF-MF) occurs from natural and artificial sources. Although ELF-MF has been classified as a suspected humans carcinogen agent by the International Agency for Research on Cancer, little is known of the effects of ELF-MF at lower exposure levels of the recommended range. In the present study, DNA damage in the peripheral blood cells of power line workers was investigated. Materials and Methods: Occupational exposure to ELF-MF in a power plant was measured using the National Institute for Occupational Safety and Health (NIOSH) manual. Single-strand breaks (SSBs) in DNA were evaluated in 29 male utility workers as the exposed population and 28 male support personnel as the control subjects using the comet assay. Effects of ELF-MF on subjects were evaluated using DNA percent in tails, tail length, olive length, and tail moment. Results: Occupational exposure levels to ELF-MF in the utility workers were less than the threshold limit values (TLV) recommended by the American Conference of Government Industrial Hygienist (ACGIH). The median value of the magnetic field at the working sites was 0.85 µT. Induction of DNA damage was observed for the exposed workers compared with the controls. Olive length, tail moment, and tail DNA percent increased significantly ( p < 0.05) in the utility workers. Conclusions: Exposure to ELF-MF at levels less than the ACGIH exposure limit can produce DNA strand breaks.

scholarly journals Regulation of Microcystin-LR-Induced DNA Damage by miR-451a in HL7702 Cells

Toxins ◽  
2019 ◽  
Vol 11 (3) ◽  
pp. 164 ◽  
Author(s):  
Lv Chen ◽  
Shu Yang ◽  
Cong Wen ◽  
Shuilin Zheng ◽  
Yue Yang ◽  
...  
Keyword(s):  
Dna Damage ◽  
Human Liver ◽  
Expression Level ◽  
Tail Moment ◽  
Protein Expression Level ◽  
Over Expression ◽  
Human Liver Cells ◽  
Normal Human Liver ◽  
Normal Human ◽  
Cyclic Heptapeptide

Microcystin-LR is a cyclic heptapeptide hepatotoxin produced by harmful cyanobacteria. A panel of microRNAs containing miR-451a were found to be significantly changed in normal human liver cells HL7702 after exposure to microcystin-LR (MC-LR) in our previous study. However, the functions of miR-451a in hepatotoxicity induced by MC-LR remained unclear. The study aimed to investigate the impacts of miR-451a in HL7702 cells following treatment with 5 or 10 μM MC-LR. The comet assay indicated that MC-LR can influence Olive tail moment (OTM) in HL7702 cells. Furthermore, increase of miR-451a significantly repressed DNA damage and the protein expression level of γ-H2AX induced by MC-LR. Moreover, over-expression of miR-451a inhibited the expression level of p-AKT1 protein in cells following treatment by MC-LR. These results showed that miR-451a may protect from MC-LR-induced DNA damage by down-regulating the expression of p-AKT1, which provides new clues for the diagnosis and therapy policies for liver damage induced by MC-LR.

scholarly journals EFFECTS OF LONG-TERM AEROBIC EXERCISE ON THE ANTIOXIDANT SYSTEM AND LYMPHOCYTE DNA DAMAGE BY TRIATHLON DISTANCE

2018 ◽  
Vol 14 (2) ◽  
pp. e42-e55 ◽  
Author(s):  
Dae-Eun Kim ◽  
Il-Young Paik ◽  
Su-Youn Cho ◽  
Jin-Hee Woo ◽  
Ju-Yong Bae ◽  
...  
Keyword(s):  
Dna Damage ◽  
Aerobic Exercise ◽  
Muscle Damage ◽  
Antioxidant System ◽  
Defense Mechanism ◽  
The Body ◽  
Blood Sampling ◽  
Medical Illness ◽  
Tail Moment

Background and Objective This study aimed to investigate the effects of long-term aerobic exercise on muscle damage markers, lymphocyte DNA damage, and antioxidant system in amateur athletes. Material and Methods Eleven healthy men in their 30s and 40s without any medical illness, who did not smoke or drink, and had completed at least two amateur triathlon races (O2 and Olympic courses) were enrolled. They underwent physical examination and four blood sampling sessions: at rest, immediately after a race, during recovery (3 and 6 days after the race), and after completing an Olympic course. Blood sampling was performed using the same method one month later. Weight (kg) and saturation of peripheral oxygen (SpO2) were measured. Tail intensity, tail moment, and tail length, and levels of superoxide dismutase (SOD), creatine kinase (CK), and lactate dehydrogenase (LDH) were analyzed. Results First, the study found significant changes between the body weight at rest and immediately after the race (p<.001) and between those immediately after the race and 3 and 6 days after the race (p<.001) for both courses. Second, for both courses, SpO2 declined immediately after the race and tended to rise again during recovery, but the difference was not significant. Third, in the Olympic course, significant differences were found between lymphocyte tail moment ™ at rest and that immediately after the race (p<.01) and between those immediately after the race and 3 and 6 days after the race (p<.05, p<.01). In the O2 course, significant differences were found between lymphocyte TM at rest and that immediately after the race (p<.01), between those at rest and 3 days of recovery (p<.001), between those immediately after the race and 3 days of recovery (p<.001), between those at rest and 6 days of recovery (p<.01), and between those at 3 and 6 days after the race (p<.01). Both courses significantly differed in lymphocyte TM immediately after the race (p<.05). Fourth, significant differences were observed between serum SOD at rest and that immediately after the race (p<.05), between those at rest and 3 days after the race (p<.01) and in serum SOD between that immediately after the race and 6 days after the race (p<.05) in the Olympic course. In the O2 course, serum SOD at rest and those at 3 and 6 days after the race significantly differed (p<.05). The two courses differed in serum SOD at 3 days after the race (p<.05). Fifth, in both courses, compared with the levels at rest, serum CK concentrations immediately after the race (p<.001) and 3 and 6 days after the race significantly differed (p<.01, p<.001). In both courses, significant differences were observed between serum CK concentrations immediately after the race and those at 3 and 6 days after the race (p<.01, p<.001) and between those at 3 and 6 days after the race (p<.001). Both courses significantly differed in serum CK concentrations immediately after the race (p<.001) and those at 3 and 6 days after the race (p<.05). In the Olympic course, serum LDH concentrations between those at rest and immediately after the race (p<.001), between those at rest and 3 days of recovery (p<.01), and between those immediately after the race and 3 and 6 days after the race showed significant differences (p<.001). In the O2 course, significant differences were found between serum LDH at rest and that immediately after the race (p<.001), between those at rest and 3 and 6 days after the race (p<.01, p<.001), between those immediately after the race and 3 and 6 days after the race (p<.001), and between those at 3 and 6 days after the race (p<.001). The two courses significantly differed in serum LDH levels immediately after the race (p<.001) and those at 3 and 6 days after the race (p<.05). Conclusion Triathlon, which involves long-term high-intensity aerobic exercise, leads to temporary weight loss, DNA damage, and muscle damage after the race, and such changes are affected by exercise duration and intensity. During this change, defense mechanisms, including the antioxidant defense mechanism, are thought to protect the body from DNA and muscle damage.

scholarly journals Electronic waste exposure and DNA damage: a systematic review and meta-analysis

2021 ◽  
Vol 0 (0) ◽  
Author(s):  
Ibrahim Issah ◽  
John Arko-Mensah ◽  
Thomas P. Agyekum ◽  
Duah Dwomoh ◽  
Julius N. Fobil
Keyword(s):  
Systematic Review ◽  
Dna Damage ◽  
Telomere Length ◽  
Chromosomal Aberrations ◽  
Electronic Waste ◽  
Meta Analysis ◽  
Waste Recycling ◽  
Tail Moment ◽  
Buccal Cells ◽  
Increased Risk

Abstract Objectives Inappropriate processing and disposal of electronic waste (e-waste) expose workers and surrounding populations to hazardous chemicals, including clastogens and aneugens. Recently, considerable literature has grown around e-waste recycling, associated chemical exposures and intermediate health outcomes, including DNA damage. Micronuclei (MN) frequency has been widely used as a biomarker to investigate DNA damage in human populations exposed to genotoxic agents. We conducted a systematic review of published studies to assess DNA damage in e-waste-exposed populations and performed a meta-analysis to evaluate the association between e-waste exposure and DNA damage. Methods This systematic review with meta-analysis was conducted following the Preferred Reporting Items for Systematic Reviews and Meta-Analysis (PRISMA) statement checklist. Articles published in English from January 2000 through December 2020 investigating the associations between e-waste exposure and DNA damage were retrieved from the following three major databases: MEDLINE, ProQuest, and Scopus. Studies that reported the use of MN assay as a biomarker of DNA damage were included for meta-analysis. Studies that also reported other DNA damage biomarkers such as chromosomal aberrations, comet assay biomarkers, 8-hydroxy-2′-deoxyguanosine (8-OHdG), telomere length, apoptosis rate were reported using narrative synthesis. Results A total of 20 publications were included in this review, of which seven studies were within the occupational setting, and the remaining 13 studies were ecological studies. The review found six biomarkers of DNA damage (micronuclei, comets assay parameters (tail length, % tail DNA, tail moment, and olive tail moment), 8-OHdG, telomere length, apoptosis rate and chromosomal aberrations) which were assessed using seven different biological matrices (buccal cells, blood, umbilical cord blood, placenta, urine and semen). Most studies showed elevated levels of DNA damage biomarkers among e-waste exposed populations than in control populations. The most commonly used biomarkers were micronuclei frequency (n=9) in peripheral blood lymphocytes or buccal cells and 8-OHdG (n=7) in urine. The results of the meta-analysis showed that electronic waste recycling has contributed to an increased risk of DNA damage measured using MN frequency with a pooled estimate of the standardized mean difference (SMD) of 2.30 (95% CI: 1.36, 3.24, p<0.001) based on 865 participants. Conclusions Taken together, evidence from this systematic review with meta-analysis suggest that occupational and non-occupational exposure to e-waste processing is associated with increased risk of DNA damage measured through MN assay and other types of DNA damage biomarkers. However, more studies from other developing countries in Africa, Latin America, and South Asia are needed to confirm and increase these results’ generalizability.

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