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Assessment of Arsenic Induced DNA Fragmentation by using Comet Assay | OMICS International
ISSN: 2157-2518
Journal of Carcinogenesis & Mutagenesis

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Assessment of Arsenic Induced DNA Fragmentation by using Comet Assay

Akram Z*, Mahjabeen I and Kayani MA

Cancer Genetics Research Group, Department of Biosciences, COMSATS Institute of Information Technology, Islamabad, Pakistan

*Corresponding Author:
Akram Z
Cancer Genetics Research Group
Department of Biosciences
COMSATS Institute of Information Technology
Islamabad, Pakistan
Tel: 092519235914
E-mail: [email protected]

Received date: February 18, 2016; Accepted date: March 16, 2016; Published date: March 18, 2016

Citation: Akram Z, Mahjabeen I, Kayani MA (2016) Assessment of Arsenic Induced DNA Fragmentation by using Comet Assay. J Carcinogene Mutagene 7:258. doi: 10.4172/2157-2518.1000258

Copyright: © 2016 Akram Z, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

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Abstract

Arsenic is metalloid present in measureable quantity in air, water, and soil through natural and anthropogenic sources. It is neurotoxic, hepatotoxic and genotoxic effects, variety of health problems have been associated to arsenic exposure. This review was designed to investigate the possible association between arsenic exposure and DNA damage in animals and humans using comet assay. Total 28 studies were selected for measuring DNA damage by comet assay. Trend of significance in tail length and tail moment was observed using regression analysis. Due to limited number of studies available the regression analysis was non-significant. Individually each study suggested a significant increase in tail moment and tail length in a dose and time-dependent manner. Overall trend observed in this review is the positive association between arsenic exposure either experimentally or occupationally and DNA damage. This initial effort may provide future guideline for the assessment of DNA fragmentation using comet assay.

Keywords

Genotoxicity; DNA damage; Comet assay; Arsenic

Introduction

Arsenic is a very common and widely distributed environmental toxicant [1] derived from natural and anthropogenic sources [2]. It can be carcinogenic depending on its exposure time, concentration, and chemical form [3]. Trivalent arsenic is 60 times more toxic than pentavalent arsenic [4,5]. Arsenic has been declared as class A human carcinogen by United States Environmental Protection Agency (EPA) [6]. At higher concentrations, arsenic acted as lethal agent, while prolonged exposure at lower concentration is associated with various human malignancies including lungs, kidneys, liver, skin abnormalities and cardiovascular diseases [1,7,8]. Underground water in many regions of the world is contaminated with high concentrations of arsenic [9]. Although United States Environmental Protection Agency (EPA) and World Health Organization (WHO) have revised drinking water standards for arsenic from 50 μg/l to 10 μg/l [6]. Millions of people are still in contact with arsenic through drinking water at concentrations greater than the standard value [10-12]. Arsenic related health problems have been reported worldwide but worst conditions have been observed in Asia, specifically in Bangladesh [3].

Arsenic is well known for the production of reactive oxygen species (ROS) [13,14]. In normal healthy body ROS and antioxidants remain in balance, and when this balance is disturbed, oxidative stress occurs [15]. Oxidative stress causes oxidative damage to cellular DNA, lipids and proteins, which contributes to cell death [16-20]. Almost 200 enzymes are inactivated by arsenic toxicity, mostly involved in DNA replication, repair and cellular energy pathways. These enzymes have greater affinity to substituted phosphate in high energy compounds as ATP results in the production of useless energy [5,21-23]. So, the genotoxicity of arsenic does not communicate directly to DNA, however, indirectly it affects DNA by production of reactive oxygen species (ROS) or deregulation of DNA repair enzymes [13,24].

Single cell gel electrophoresis or comet assay is widely accepted as a simple, sensitive and standard technique for the detection of DNA damage at single cell level. Genotoxicity of various industrial chemicals, agrochemicals, pharmaceuticals and pollutants can be assessed with comet assay [25]. This assay can detect DNA damage in different cell types such as in skeletal muscle cells [26], cumulus cells [27], eosinophils [28] and ovarian cells [29]. It has also been used to detect DNA damage in blood of Polish copper smelter workers occupationally exposed to inorganic arsenic [30].

The association between arsenic exposure and DNA damage is a matter of concern. Purpose of this review is to provide quantitative estimate of DNA damage in subjects exposed to arsenic either experimentally/cell lines, occupationally or naturally. Main focus of present review was based on potential relationship between the arsenic concentration, exposure time, and DNA damage which was detected by comet assay.

Methodology

The aim of present review is to investigate the toxic effects of arsenic on DNA fragmentation in blood, liver, reproductive organs and in different types of cell lines.

Literature search

A comprehensive search strategy was used to identify all the related studies. Database of Pubmed from 2000-2015 was searched and following key words were used: comet assay, blood, liver tissue, ovarian tissue, testicular tissue and arsenic induced DNA damage. The search was restricted to English language. Only full length articles were included, unpublished data and abstracts were not considered.

Inclusion and exclusion criteria

The following inclusion criteria are used to select articles for this review: (1) studies using both human and animal models were included (2) studies using the evaluation of DNA fragmentation by comet assay were included (3) studies using the assessment of arsenic genotoxicity in liver, blood, ovarian, testicular tissues and cell lines were also included in this review. Exclusion criteria used for this review as follows: (1) studies assessing the DNA damage by techniques other than comet assay were not included in this study(2) studies on metals other than arsenic were excluded (3) abstracts were also excluded from this analysis.

Statistical analysis

Data are expressed as Mean ± SEM. Exposure time and doses were considered. Different parameters of comet assay were measured in twenty eight studies of this review. In thirteen studies (11 for blood, 1 for liver, 1 for ovary: (Table 1) the statistical values were given for comet parameter. Arsenic induced DNA damage in cell lines of different cancers was studied in fifteen studies. Regression analysis was performed to assess the correlation between exposure time and comet parameters (tail length and tail moment) (Table 1).

No. Author Year Model Tissue Observed parameter
1 Flora et al. [31-32] 2004 Rat Blood Tail length
2 Yanezet al.[33] 2003 Human Blood Tail length, tail moment
3 Vuyyuriet al. [34] 2006 Human Blood Tail length
4 Banerjee et al.[35] 2008 Human Blood %tail DNA, olive tail moment,tail length
5 Ahmad et al.[36-39] 2011 Fish Liver % tail DNA
6 Basuet al.[24] 2005 Human Blood %tail DNA, tail length,tailmoment,comet length
7 Paluset al. [30] 2005 Human Blood Tail moment
8 Paluset al.[38] 2006 Mice Blood Tail moment
9 Mendez-Gomez et al.[36] 2008 Human Blood Tail length
10 Akramet al.[29] 2009 Rat Ovary %DNA tail, tail length,tailmoment,olive tail moment
11 Ahmad et al.[36-39] 2011 Fish Liver % tail DNA
12 Ahmad et al.[39] 2011 Fish Blood % tail DNA
13 Flora et al.[32] 2012 Mice Blood Tail length
14 Jasso-Pineda [37] 2012 Human Blood Tail moment

Table 1: Characteristics of studies having arsenic induced DNA damage assessed by comet assay.

Results

Literature survey

This database yielded total 3316 articles for comet assay in blood, liver tissues, ovarian tissue, testicular tissue and cell lines. Of the retrieved articles 3277 were research articles while 39 were review articles. Most of the review articles were relevant to blood and cell lines and only 2 were related to liver. These 39 review articles were excluded from the present study.

Remaining 3277 articles were investigated to sort out the data for blood, liver, ovarian, testicular tissue and cell lines. Out of which we found 2707 articles for blood, 277 for liver tissue, 6 for ovarian tissue, 14 for testicular tissue and 273 for cell lines. In 273 articles of cell lines only 165 human related articles were investigated, out of which just 56 articles were found with full text. Next major step was to extract arsenic related data from these articles. A total of 82 articles were relevant to arsenic, in which twenty one studies used blood, three used liver tissue, one used ovarian tissue, one for testicular tissue and 56 for cell lines. In twenty one articles of blood, ten were excluded from the study, six were abstracts, two articles were in Chinese language, and two articles used cell culture for damage assessment. Therefore, a total of eleven articles were selected for comet assay in blood. In liver tissue three relevant articles were found, of which two were excluded one was abstract and other article was an in-vitro study. Therefore only one article was selected for liver tissue. We found only one article for ovarian tissue and one for testicular tissue for this study, but article of testicular tissue was excluded because of the availability of abstract only. Fifty six articles were retrieved for cell lines of different cancers. Out of which 41 were non-related to study criteria, they were excluded and only fifteen articles of cell lines were selected for this study. Thus, a total of twenty eight studies: eleven blood study, one liver and one ovarian tissue and fifteen cell lines study were included in this review (Figure 1).

carcinogenesis-mutagenesis-inclusion-criteria

Figure 1: Flow chart showing exclusion inclusion criteria of studies used in this review.

Characteristics of study

Total twenty eight studies were included in this review and these were not confined to any particular experimental model. Fifteen studies were related to cell line and remaining thirteen were related to blood/tissue. Regression analysis was done in thirteen studies (Table 1). Among which seven studies have reported different parameters of comet assay in blood of humans. Two studies have been reported for blood of mice, one for rat and one for fish sample. One study has been reported for ovarian tissue of rat and one for liver of fish. The study of Ahmad et al. has been shown twice because it contained data both for blood and liver tissue. In all these studies different parameters of comet assay has been observed in order to evaluate DNA fragmentation induced by arsenic toxicity either by experimental mean or by living in natural environment. Major comet parameters used in these studies, as a marker of DNA damage, are comet tail length, tail moment and %tail DNA. In remaining 15 studies of cell lines, different comet parameters were studied but statistical values were not given, rather data was presented either in graphical form or as a photograph of comet to show the intensity of DNA damage in theses cell lines. Due to lack of sufficient statistical values no further analysis was made between these studies.

Detail description of findings

Detailed description of thirteen studies of blood and tissues included in this review is given in Table 2. Two studies of Flora et al. [31,32] are included in this study. Significant DNA damage was assessed in mice [32], while in rats no data was reported [31]. Similar extent of DNA damage was observed in children living in mining site of Villa de Paz with high arsenic contamination compared with children living in Matechuala with low arsenic contamination [33]. People of West Bengal have high arsenic exposure and therefore express significant DNA damage in blood compared to unexposed or less exposed population [24]. Poland and South Indian population are occupationally exposed to arsenic and have shown DNA fragmentation compared to unexposed population [30,34]. People of India (Murshidabad) exposed to arsenic contaminated drinking water express greater extent of DNA migration compared to unexposed population [35]. Mendez-Gomez et al. [36] and Jasso-Pineda et al. [37] studied different arsenic exposed areas in Mexico and observed greater fragmentation of DNA damage in areas located nearest to arsenic source (Table 2).

Number Author Year Model Tissue Doses/area Exposure Comet parameter Mean Observed effects
1 Flora et al. [31] 2004 Rat Blood 10mgKg-1 5days/wk/12wk tail length no data heavy DNA damage
2 Yanezet al. [33] 2003 Human Blood Villa de la Paz ±2years tail length, tail moment 67.6µm, 6.8 significant damage
          Matehuala     41.7µm, 3.2 in Villa de la Paz
3 Basuet al. [24] 2005 Human Blood West Bengal ±5years %DNA tail 59.74±10.54µm  
              Tail length 58.68±10.23µm DNA damage
              Tail moment 42.31±11.58  
              Comet length 83.33±15.51µm  
4 Paluset al. [30] 2005 Human Blood Poland ±18years Tail moment 13.2x10-3 significant damage
5 Paluset al.[38] 2006 Mice Blood 50µg/L 3,6,12 months Tail moment 0.14±0.11,0.02±0.02,0.14±0.07 significant damage
          200µg/L 3,6,12 months   0.16±0.12,0.03±0.01,0.02±0.01 at 50µg/L
          500µg/L 3,6,12 months   0.12±0.06,0.03±0.01,0.03±0.03  
6 Vuyyuriet al.[34] 2006 Human Blood India minimum 3 year Tail length 14.95±0.21µm signficant damage
7 Banerjee et al. [35] 2008 Human Blood Murshidabad ±10year Olive tail moment 2.76±1.39 significant damage
              %DNA tail 14.05±4.71  
              Tail length 11.85±5.51  
8 endez-Gomez et al.[36] 2008 Human Blood Mexico(3 school around arsenic location) minimum 6 month Tail length    
          Distant     29.2 significant damage
          Intermediate     25.3 in nearest compared
          Nearest     28.6 to intermediate
9 Akramet al.[29] 2009 Rat Ovary 50,100,200ppm 28 days Tail moment 0.09±0.01,0.45±0.05,0.50±0.05 significant damage
              Tail length 17.98±1.39, 20.61±1.45,22.12±1.49 maximum at high dose
              %DNA tail 0.43±0.02,1.73±0.08,2.12±0.11  
              Olive tail moment 0.08±0.01,0.40±0.04,0.50±0.04  
10 Ahmad et al. [39] 2011 Fish Liver 3ppm 48,96,192hrs %DNA in tail >10, >20, >20 significant, with
          28ppm     >30, >40, >30 maximum damage
          56ppm     >40, >50, >40 at 96hr
11 Ahmad et al. [39] 2011 Fish Blood 3ppm 48,96,192hrs %DNA tail >10, >10, >10 significant, with
          28ppm     >20, >30, >20 maximum damage
          56ppm     >30, >40, >30 at 96hr
12 Flora et al.[32] 2012 Mice Blood 5mg l-1 28 weeks Tail length >150µm significant damage
13 Jasso-Pineda [37] 2012 Human Blood San Luis Potosi state(3 communities)        
          community 1 ±6year Tail moment 5.2±0.6 significant damage
          community 2 ±6year   3.5±0.4  
          community 3 ±7year   2.5±0.4  

Table 2: Detailed description of findings observed in present review.

Arsenic induced genotoxicity has also been calculated in animals exposed to different doses of arsenic and significant DNA damage has been observed in mice [38] rats [29], and fish [39].

Arsenic is involved in the promotion of different cancers. Therefore, cell lines of different cancer were investigated. Fifteen studies in different cell lines were included in this review (Table 3).

No Author Sample Arsenic species Dose /Exposure
1 Gattiet al., 2014 [40] non smal cell lung cancer A549 Arsenic trioxide 80µM, 3hrs
2 Yooet al., 2009 [41] HCC cell line SK-Hep-1 Sodium arsenite 2μM, 48 h
3 Yedjou and Tchounwou, 2007 [42] HL-60 promyelocyticleukemia cell line Arsenic trioxide 10 μg/mL
4 Doppet al., 2008 [43] Primary human hepatocytes Sodium arsenite/arsenate 0.1-500μM, 1 hr
5 Graham et al., 2014 [44,45] Induced plurpotent stem cell (IPS) Arsenic trioxide 1,3,5,7,9µg/ml, 24hrs
6 Jan et al., 2006 [46] NB4- human promyelocyticleukemia cell line Arsenic trioxide 1μM
7 Kryeziuet al., 2013 [47] NSCLC cell lines A549 Arsenic trioxide 100µmol/L, 6hrs
8 Liu et al., 2010 [48] glioblastoma multiforme U87 cells Arsenic trioxide 6μM, 4 h
9 Nakamura et al., 2013 [49] osteosarcoma cell line 143B Arsenic trioxide 3µM
10 Puet al., 2007 [50] NB4-human promyelocyticleukemia cell line Sodium arsenite 0.2μM, 1 h and 24hrs
11 Qin et al., 2008 [51] human keratinocyte cell line (HaCat) Sodium arsenite 10μM, 24 hrs
12 Stevens et al., 2010 [52] Human colon cancer (HT-29) Arsenic trioxide 2,4,6,8,10,12 μg/mL, 24 h
13 3 Wnecket al., 2011 [53] bladder urothelial cells (UROtsa) Monomethylarsonous acid 50 nM, 12 weeks
14 Xieet al., 2014 [2] lung fibroblast/epithelial cells Sodium arsenite 0.5,1,5,10µM, 24/120hrs
15 Chai et al., 2007 [8] Human uroepithelial cell line (SV-HUC-1) Sodium arsenite 1, 2, 4, 8, 10 μM, 48hrs

Table 3: Detailed description of cell lines studies selected for this review.

In all these studies positive trend of DNA damage with increased doses of arsenic exposure was reported. Most of the data was presented as a graph or picture to show the DNA fragmentation. Only four authors had given values for tail length and tail moment [8,40-42]. DNA damage was increased with increasing dose of arsenic (Table 4).

Author Year Cell line s Come t Parameter
      Tail length Tail moment
Gattiet al.[40] 2014 Nonsmal cell lung cancer A549 _ 9.07, 7.23
Yooet al.[41] 2009 HCC cell line SK-Hep-1 255.92 136.23
Chai et al.[8] 2007 Human uroepithelial cell line (SV-HUC-1) 65.91, 71.27, 98.01 _
Yedjou and Tchounwou [42] 2007 HL-60 promyelocyticleukemia cell line 3, 17, 24 _

Table 4: Statistical values of comet parameters in cell lines of different cancers.

Statistical facts

This review is not confined to any specific experimental model. Human, rats, mice and fish have been used as a model in selected studies. Humans had natural exposure or occupational exposure to arsenic by living or working in that particular environment. In seven studies of human population of different arsenic contaminated areas, arsenic exposure ranged from 6 months to 18 years. Among which only in one study, the exposure time was not been reported [37]. In these seven studies significant increase has been reported in comet tail length and tail moment of exposed individuals compared to unexposed or less exposed individuals. Comet tail length and tail moment in different populations of exposed areas is shown in figure 2 observed in this review.

carcinogenesis-mutagenesis-tail-length

Figure 2: Overall relationship between tail length (A), tail moment (B) and exposure time in different populations.

Regression analysis was performed in studies of human population to assess the correlation between exposure time and extent of DNA damage in exposed individuals. Regression analysis is shown in figure 3. Regression analysis in human samples revealed a non-significant relationship between exposure time and comet parameters. Regression analysis was not performed for animal studies because of very few studies found; only one study was reported for blood of mice, ovarian tissue of rat and blood and liver tissue of fish. In these three studies animals were exposed to different doses of arsenic for different time periods. Although the parameters of comet varied in these studies but individually each study suggested a significant damage with high doses compared to low doses (Figure 3).

carcinogenesis-mutagenesis-human-samples

Figure 3: Calculated regression line showing non-significant relation between exposure time to arsenic and comet parameters in human samples.

The complete picture of arsenic deposition either in blood, water, urine, or tissue observed in this review is shown in table 5. In six studies arsenic deposition was measured in urine, in 3 studies arsenic was measured in blood and water and in one study arsenic was measured in ovary, liver, nail, hair, dust and soil sample. In observed studies arsenic deposition differed in different samples with respect to the doses for animals and with respect to the location of arsenic for human population. Marked relationship can be observed between the deposition of arsenic and DNA fragmentation in comet tail length and tail moment (Table 5).

Number Author Year Model Area Exposure Dose Arsenic concentration Comet parameter
              dust/soil water urine blood liver ovary tail length tail moment
1 Flora et al. [31] 2004 Rat _ 12wk 10mgKg-1       3.5µg/ml 2.5µg/g _ _ _
2 Yanezet al.[33] 2003 Human Villa de la Paz ±2years _ 2462mg/kg   136µg/gc _ _ _ 67.6 6.8
        Matehuala   _ 1019mg/kg   34µg/gc _ _ _ 41.7 3.2
3 Basuet al.[24] 2005 Human West Bengal ±5years _ _ 247.12µg/L 259.75µg/L _ _ _ 58.68 42.31
4 Paluset al.[30] 2005 Human Poland ±18years _ _   60µg/L _ _ _ _ 13.2
5 Vuyyuriet al. [34] 2006 Human India min 3 year _ _     56.76µg/L _ _ 14.95 _
6 Banerjee et al.[35] 2008 Human Murshidabad ±10year _ _ 5.04µg/L 296.03µg/L   _ _ 11.85 _
7 Mendez-Gomez et al. [36] 2008 Human Mexico(around arsenic location) min 6 month   µg/g µg/L µg/L       _ _
        Distant _ _ 21.8 26.05 143 _ _ _ 29.2 _
        Intermediate _ _ 75.6 6.8 100 _ _ _ 25.3 _
        Nearest _ _ 155.6 13.16 115 _ _ _ 28.6 _
8 Akramet al. [29] 2009 Rat _ 28days 50ppm _ _ _ _ _ 1µg/mg 17.9 0.09
        _ _ 100ppm _ _ _ _ _ 1-2µg/mg 20.61 0.45
        _ _ 200ppm _ _ _ _ _ 3-4µg/mg 22.12 0.5
9 Flora et al. [32] 2012 Mice _ 28 wk 5mg l-1 _ _   7-8ng/ml-1 5-6µg/g-1   100-150 _
10 Jasso-Pineda [37] 2012 Human San Luis Potosi state         µg/gc         _
        community 1(nearest) ±6years _ _ _ 44.5 _ _ _ _ 5.2
        community 2(inter) ±6years _ _ _ 16.8 _ _ _ _ 3.5
        community 3(distant) ±7years _ _ _ 12.8 _ _ _ _ 2.5

Table 5: Arsenic deposition in different biological samples estimated in studies of present review.

Discussion

In this review, arsenic induced genotoxocity was measured by comet assay in blood/tissue sample or cell lines. The in-vivo or invitro genotoxicity induced by different ways chemicals, pesticides, insecticides, environmental pollutants, or endocrine disruptors has been widely studied by using comet assay [25]. The most frequent parameter used to measure DNA damage was comet tail length and tail moment.

This review has explored the association of arsenic exposure and DNA fragmentation in humans, animal model and in cell lines. In human studies the population is chronically and naturally exposed to arsenic either by living in close proximity to arsenic source, by drinking arsenic contaminated water, by inhaling the arsenic dust or occupationally exposed to arsenic. The animals are exposed to different doses. Dose, concentration, exposure time, distance affects the arsenic induced genotoxicity. DNA damage has been detected in ovarian tissue in a dose-dependent manner [29]. Similarly higher extent of DNA fragmentation has also been reported in different communities of San Luis Potosi State [37] and in different schools of Mexico [36] located at different distances from arsenic smelter area.

Major limitation in this review is the limited number of studies examining the association of arsenic exposure and DNA fragmentation. In human studies, DNA damage was measured by comet assay only in blood sample, and there was no tissue related study. In six studies of animals, four were carried out in blood sample, one in ovarian tissue and only one in liver tissue. While in cell line studies only four had shown the statistical values of comet assay indicating DNA damage, while in remaining eleven studies DNA damage was expressed either as a graph or microphotograph. Due to lack of statistical data it is not possible to perform any further analysis in cell line studies. Regression analysis was performed in human studies to correlate time exposure and DNA damage, which was statistically non-significant. Nevertheless, each study has shown greater extent of DNA damage in exposed individuals compared to unexposed or less exposed population(s). The difference was even clear when two areas of same city were considered, which were located at variable distance from arsenic source.

Animal studies were not enough in number to perform statistical analysis. There was only single study evaluating DNA damage in ovarian tissue of rat [29] and in liver of fish [39] exposed to different doses of arsenic and indicated the increased extent of DNA damage with all doses, specifically at high dose levels. In studies of current review, arsenic concentration was measured in blood, liver, ovary and water. Levels of arsenic in these measured parameters has shown greater extent of deposition in region closely located to arsenic source in case of human and with high doses in case of experimental animals.

Present study suggests a possible association between arsenic exposure and DNA damage either in humans, experimental animals or in cell lines. Overall trend from all the studies propose that the genotoxicity of arsenic is dose-dependent as well as time-dependent. Nevertheless, small numbers of studies are the limitation factor to illuminate the complete and clearer picture of arsenic genotoxicity but this initial effort can make a future guideline for the assessment of DNA fragmentation using comet assay.

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Review summary

  1. Dominique
    Posted on Jul 20 2016 at 2:31 pm
    This authors discuss a highly important subject which is worthy of review and discussion. The authors concluded that almost all studies on arsenic confer the genotoxicity of arsenic is dose-dependent as well as time-dependent manner. The article highlights a future guideline for the arsenic induced DNA fragmentation assessment using comet assay.
  2. Rose M
    Posted on Jul 14 2016 at 11:36 pm
    This subject is worthy of review and discussion. The authors have done comprehensive study on arsenic toxicity on DNA damage. The overall conclusion is acceptable "Overall trend from all the studies propose that the genotoxicity of arsenic is dose-dependent as well as time-dependent" and "a future guideline for the assessment of DNA fragmentation using comet assay".

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