DNA Damage Scores Research Articles

Isolation and comparative genotoxicity screening of trichokonins VI and VIII on CHO-K1 cells

Peptaibols are fungal peptides that exhibit efficacy against pathogen microorganisms. Trichokonin VI (TK-VI) and trichokonin VIII (TK-VIII) are known peptaibols isolated from the endolichenic fungi Hypocrea sp. Previous investigations reported that trichokonin VI presents antiproliferative effects on tumor cells. This study is pioneering in elucidating the genotoxic effects of TK-VI and TK-VIII, contributing to the thorough assessment of their safety as potential therapeutic agents. The present investigation aimed to evaluate the genotoxicity of TK-VI and TK-VIII on CHO-K1 cells. Cytotoxicity was evaluated using the XTT assay and clonogenic survival assays, followed by evaluation of DNA damage using the comet assay and micronucleus test conducted in vitro. The XTT assay results indicated IC50 values of 10.30 µM and 9.89 µM for TK-VI and TK-VIII, respectively. The clonogenic survival assay indicated that concentrations of 10 µM or higher completely inhibited the cell colony formation. In the comet assay, both TK-VI and TK-VIII increased the DNA damage score and the frequency of comet nuclei in all tested concentrations. In the micronucleus assay, TK-VI and TK-VIII at 10 µM increased the frequency of MN in CHO-K1 cells. Both TK-VI and TK-VIII exhibited genotoxic effects. Our findings underscore the importance of considering the genotoxicological safety of peptaibols, particularly when assessing their potential for other biological activities.

DNA fragmentation and multifaceted toxicity induced by high-dose vanadium exposure determined by the bioindicator Allium test

In this study, the toxicity of vanadium (VCI3) in Allium cepa L. was studied. Germination-related parameters, mitotic index (MI), catalase (CAT) activity, chromosomal abnormalities (CAs), malondialdehyde (MDA) level, micronucleus (MN) frequency and superoxide dismutase (SOD) activity were investigated. The effects of VCI3 exposure on the DNA of meristem cells were investigated with the help of comet assay, and the relationships between physiological, cytogenetic and biochemical parameters were revealed by correlation and PCA analyses. A. cepa bulbs were germinated with different concentrations of VCI3 for 72 h. As a result, the maximum germination (100%), root elongation (10.4 cm) and weight gain (6.85 g) were determined in the control. VCI3 treatment caused significant decreases in all tested germination-related parameters compared to the control. The highest percentage of MI (8.62%) was also observed in the control. No CAs were found in the control, except for a few sticky chromosomes and unequal distribution of chromatin (p > 0.05). VCI3 treatment caused significant decreases in MI and increases in the frequencies of CAs and MN, depending on the dose. Similarly, the comet assay showed that DNA damage scores increased with increasing VCI3 doses. The lowest root MDA (6.50 µM/g) level and SOD (36.7 U/mg) and CAT (0.82 OD240nmmin/g) activities were also measured in the control. VCI3 treatment caused significant increases in root MDA levels and antioxidant enzyme activities. Besides, VCI3 treatment induced anatomical damages such as flattened cell nucleus, epidermis cell damage, binuclear cell, thickening in the cortex cell wall, giant cell nucleus, damages in cortex cell and unclear vascular tissue. All examined parameters showed significant negative or positive correlations with each other. PCA analysis confirmed the relations of investigated parameters and VCI3 exposure.

Assessment of Neurotoxic Effects of Oxycodone and Naloxone in SH-SY5Y Cell Line.

Opioid drugs have analgesic properties used to treat chronic and post-surgical pain due to descending pain modulation. The use of opioids is often associated with adverse effects or clinical issues. This study aimed to evaluate the toxicity of opioids by exposing the neuroblastoma cell line (SH-SY5Y) to 0, 1, 10, and 100 µM oxycodone and naloxone for 24 h. Analyses were carried out to evaluate cell cytotoxicity, identification of cell death, DNA damage, superoxide dismutase (SOD), glutathione S-transferase (GST), and acetylcholinesterase (AChE) activities, in addition to molecular docking. Oxycodone and naloxone exposure did not alter the SH-SY5Y cell viability. The exposure to 100 µM oxycodone and naloxone significantly increased the cells' DNA damage score compared to the control group. Naloxone exposure significantly inhibited AChE, GST, and SOD activities, while oxycodone did not alter these enzymes' activities. Molecular docking showed that naloxone and oxycodone interact with different amino acids in the studied enzymes, which may explain the differences in enzymatic inhibition. Naloxone altered the antioxidant defenses of SH-SY5Y cells, which may have caused DNA damage 24 h after the exposure. On the other hand, more studies are necessary to explain how oxycodone causes DNA damage.

Bioaccumulation, cytotoxicity and oxidative stress of the acute exposure selenium in Oreochromis mossambicus

Selenium (Se) is an essential trace-element that becomes toxic when present at high concentrations for aquatic organisms. The knowledge about the mechanism of Se toxicity in freshwater ecosystem is still poorly studied. Thus the aim of the present study was to assess the impact of environmentally relevant concentrations of Se toxicity: 5, 10, 25, 50 and 100 µg/L or water only (control) for periods of 96 hour (h) to test for Se accumulation (gill, liver and brain), its effects on enzymatic and non-enzymatic antioxidant defenses (gill and liver), oxidative stress effects on lipid, protein (gill and liver), DNA (liver) and inhibition of AchE (brain) activity were measured in Mozambique tilapia, Oreochromis mossambicus. Our result showed that Se accumulation was observed in the gill, liver and brain tissues of fish exposed to different concentrations and accumulation varied upon different tissues. Enzymatic (SOD, CAT, GPx and GST) and non-enzymatic (GSH and MT) antioxidant enzymes such as superoxide dismutase (SOD), glutathione peroxidase (GPx) and glutathione-s-transferase (GST) were significantly increased after 96 h exposure of higher concentrations Se in the gill and liver tissue with the exception of GST activity was significantly inhibited in liver after 96 h exposure of higher concentrations of Se. In contrast, catalase (CAT) activities were inhibited for both tissues of Se exposure at 96 h. Reduced glutathione (GSH) and Metallothionein (MT) levels were increased in the gill and liver tissues after exposure to Se for 96 h. We also observed that Se affected antioxidant defense, increasing oxidative stress indicator of lipid peroxidation (LPO) and protein carbonyl (PCO) in gill and liver tissues of fish exposed to Se for 96 h at the concentration dependent manner. Increased DNA damage scores observed in liver tissue of fish exposed to Se for concentrations dependent manner, indicating potential of Se on fish. We also observed inhibition of acetylcholine esterase (AchE) activity in brain tissue of fish exposed to Se for higher concentrations. The changes in these parameters can be used as suitable biomarkers for monitoring the toxicity of Se in the aquatic environment.

Quantification of glucosylshingosine (lyso-Gb1) for the diagnosis and monitoring of Gaucher disease

Miltefosine was developed to treat skin cancer; further studies showed that the drug also has activity against Leishmania. Miltefosine is the first oral agent for treating leishmaniasis. However, its mechanism of action is not completely understood. We have evaluated the induction of DNA damage by miltefosine. Cytotoxicity and genotoxicity (comet assay) tests were performed on human leukocytes exposed to the drug in vitro. Apoptosis and necrosis were also evaluated. In vivo tests were conducted in Swiss male mice (Mus musculus) treated orally with miltefosine. Oxidation of DNA bases in peripheral blood cells was measured using the comet assay followed by digestion with formamidopyrimidine glycosylase (FPG), which removes oxidized guanine bases. The micronucleus test was performed on bone marrow erythrocytes. Miltefosine caused DNA damage, apoptosis, and necrosis in vitro. Mice treated with miltefosine showed an increase in the DNA damage score, which was further increased following FPG digestion. The micronucleus test was also positive.

Oxidative status and reduced glutathione levels in premature coronary artery disease and coronary artery disease

Identifying patients at risk of developing premature coronary artery disease (PCAD) which occurs at age below 45 years old and constitutes approximately 7–10% of coronary artery disease (CAD) worldwide remains a problem. Oxidative stress has been proposed as a crucial step in the early development of PCAD. This study was conducted to determine the oxidative status of PCAD in comparison to CAD patients. PCAD (<45 years old) and CAD (>60 years old) patients were recruited with age-matched controls (n = 30, each group). DNA damage score, plasma malondialdehyde (MDA) and protein carbonyl content were measured for oxidative damage markers. Antioxidants such as erythrocyte glutathione (GSH), oxidised glutathione (GSSG), and glutathione peroxidase activity (GPx), superoxide dismutase (SOD) and catalase (CAT) were also determined. DNA damage score and protein carbonyl content were significantly higher in both PCAD and CAD when compared to age-matched controls while MDA level was increased only in PCAD (p<.05). In contrast, GSH, GSH/GSSG ratio, α-tocotrienol isomer, and GPx activity were significantly decreased, but only in PCAD when compared to age-matched controls. The decrease in GSH was associated with PCAD (OR = 0.569 95%CI [0.375 − 0.864], p = .008) and cut-off values of 6.69 μM with areas under the ROC curves (AUROC) 95%CI: 0.88 [0.80–0.96] (sensitivity of 83.3%; specificity of 80%). However, there were no significant differences in SOD and CAT activities in all groups. A higher level of oxidative stress indicated by elevated MDA levels and low levels of GSH, α-tocotrienol and GPx activity in patients below 45 years old may play a role in the development of PCAD and has potential as biomarkers for PCAD.

An extended one-generation reproductive toxicity study of plant protection product containing glyphosate on rats – Androgen- and estrogen-dependent endpoints

Roundup Transorb® (RT) is a glyphosate-based herbicide and despite its wide use around the world there are few studies comparing the effects of the active ingredient with the formulated product. In this context the purpose of this study was to compare the genotoxicity of the active ingredient glyphosate with the formulated product RT in order to clarify whether the active ingredient and the surfactant of the RT formula may exert toxic effects on the DNA molecule in juveniles of fish Prochilodus lineatus. Erythrocytes and gill cells of fish exposed to glyphosate and to RT showed DNA damage scores significantly higher than control animals. These results revealed that both glyphosate itself and RT were genotoxic to gill cells and erythrocytes of P. lineatus, suggesting that their use should be carefully monitored considering their potential impact on tropical aquatic biota.

The antileishmanial drug miltefosine (Impavido®) causes oxidation of DNA bases, apoptosis, and necrosis in mammalian cells

Miltefosine was developed to treat skin cancer; further studies showed that the drug also has activity against Leishmania. Miltefosine is the first oral agent for treating leishmaniasis. However, its mechanism of action is not completely understood. We have evaluated the induction of DNA damage by miltefosine. Cytotoxicity and genotoxicity (comet assay) tests were performed on human leukocytes exposed to the drug in vitro. Apoptosis and necrosis were also evaluated. In vivo tests were conducted in Swiss male mice (Mus musculus) treated orally with miltefosine. Oxidation of DNA bases in peripheral blood cells was measured using the comet assay followed by digestion with formamidopyrimidine glycosylase (FPG), which removes oxidized guanine bases. The micronucleus test was performed on bone marrow erythrocytes. Miltefosine caused DNA damage, apoptosis, and necrosis in vitro. Mice treated with miltefosine showed an increase in the DNA damage score, which was further increased following FPG digestion. The micronucleus test was also positive.

Effects of Vitamin B12 in Neonates and Young Infants

Vitamin B12 (cobalamin) is an essential coenzyme for nucleic acid synthesis. Animal protein is the major dietary source of vitamin B12. Deficiency of vitamin B12 leads to megaloblastic anemia, degeneration of the brain, spinal cord, peripheral nerves, and abnormalities of epithelial tissues. Two factors are necessary for the cure of megaloblastic anemia: one in food (extrinsic factor) and one in gastric juice (intrinsic factor). The extrinsic factor is vitamin B12. Intrinsic factor (a glycoprotein secreted by gastric parietal cells) ensures cobalamin absorption by receptors in the terminal ileum. Vitamin B12 is actively transported across the placenta. Neonates have high serum levels and significant liver stores of vitamin B12. The neonates born to mothers with deficiency of vitamin B12 have deficiency of this vitamin. Pregnant women in resource-poor areas have low vitamin B12 status which is associated with adverse pregnancy outcomes, including anemia, low birth weight, and intrauterine growth retardation. Supplementation of vitamin B12 had significantly higher plasma of vitamin B12 in mothers and neonates. A single intramuscularly injection of vitamin B12 of between 250 µg and 1mg and a dietary intake of 1 µg/kg per day vitamin B12 is sufficient to combat vitamin B12 deficiency. Mean DNA damage scores in infants with vitamin B12 deficiency and their mothers were significantly higher before than after supplementation with vitamin B12. There were correlations between the infants' and their mothers' DNA damage scores. The aim of this study is the review of the effects of vitamin B12 in neonates and young infants.

Biomarkers of waterborne copper exposure in the Neotropical fish Prochilodus lineatus

The main goal of the present study was to investigate the effects of acute exposure to copper (Cu) using a Neotropical freshwater fish as sentinel species through multi biomarkers analysis at different biological levels. Juveniles of Prochilodus lineatus were kept under control condition (no Cu addition in the water) or exposed to environmentally relevant concentrations of waterborne Cu (5, 9 and 20μgL−1) for 96h. These concentrations were selected to bracket the current Brazilian water quality criteria for Cu in fresh water (9 and 13μgL−1 dissolved copper). Endpoints analyzed included ethoxyresorufin-O-deethylase (EROD), glutathione-S-transferase (GST), catalase (CAT), glutathione peroxidase (GPx) and superoxide dismutase (SOD) activity, reduced glutathione (GSH) and metallothionein-like protein (MT) concentration, lipid peroxidation (LPO) level, tissue damage index, and incidence of free melano-macrophages (FMM) and melano-macrophage centers (MMC) in the liver. They also included DNA damage (frequency of nucleoids per comet class, number of damaged nucleoids per fish and DNA damage score) in erythrocytes, as well as muscle and brain acetylcholinesterase (AChE) activity and behavioral parameters (swimming distance and velocity, time spent swimming and swimming activity in the upper and lower layers of the water column). Fish exposed to any of the Cu concentrations tested showed increased liver MT concentration and LPO level, higher number of damaged nucleoids in erythrocytes per fish, and inhibited muscle AChE activity. Also, increased liver SOD activity was observed in fish exposed to 9 and 20μgL−1 Cu. Fish exposed to 5 and 9μgL−1 Cu spent lower amount of time swimming. Fish exposed to 9μgL−1 Cu showed increased swimming distance and velocity while those exposed to 20μgL−1 Cu had lower swimming distance and velocity, as well as, spent less time swimming in the lower layer of the water column when compared to those kept under control condition. These findings indicate that Cu exposure at environmentally relevant concentrations (below or close to the current Brazilian water quality criteria) induced significant biological (histological, biochemical and genetic) and ecological (swimming and exploratory abilities) damages in the Neotropical fish P. lineatus. They also suggest that MT concentration, DNA damage (comet assay), LPO (TBARS method), SOD and AChE activity, together with swimming behavior analyses are potential biomarkers to assess and monitor areas impacted by Cu in fresh water.

Oxidative DNA Damage, Oxidative Stress and Genetic Susceptibility-Prognostic Scores in ‘Missing’ COPD Cases

In situ identification of COPD cases at workplace and sample assessment for oxidative stress/ DNA damage as a function of metabolic/antioxidant genotypes (as susceptibility genotypes) offers a nove...

Evaluation of drinking water treatment combined filter backwash water recycling technology based on comet and micronucleus assay

Based on the fact that recycling of combined filter backwash water (CFBW) directly to drinking water treatment plants (WTP) is considered to be a feasible method to enhance pollutant removal efficiency, we were motivated to evaluate the genotoxicity of water samples from two pilot-scale drinking water treatment systems, one with recycling of combined backwash water, the other one with a conventional process. An integrated approach of the comet and micronucleus (MN) assays was used with zebrafish (Danio rerio) to investigate the water genotoxicity in this study. The total organic carbon (TOC), dissolved organic carbon (DOC), and trihalomethane formation potential (THMFP), of the recycling process were lower than that of the conventional process. All the results showed that there was no statistically significant difference (P>0.05) between the conventional and recycling processes, and indicated that the genotoxicity of water samples from the recycling process did not accumulate in 15day continuous recycling trial. It was worth noting that there was correlation between the concentrations of TOC, DOC, UV254, and THMFPs in water and the DNA damage score, with corresponding R2 values of 0.68, 0.63, 0.28, and 0.64. Nevertheless, both DNA strand breaks and MN frequency of all water samples after disinfection were higher than that of water samples from the two treatment units, which meant that the disinfection by-products (DBPs) formed by disinfection could increase the DNA damage. Both the comet and MN tests suggest that the recycling process did not increase the genotoxicity risk, compared to the traditional process.

Oxidative DNA Damage, Oxidative Stress and Genetic Susceptibility-Prognostic Scores in ‘Missing’ COPD Cases

KEYWORDS Genetic Polymorphism. Glutathione-S-Transferase. 8-OHdG. Stone-crushing Superoxide Dismutase ABSTRACT In situ identification of COPD cases at workplace and sample assessment for oxidative stress/ DNA damage as a function of metabolic/antioxidant genotypes (as susceptibility genotypes) offers a novel manner of hazardous workplace-identification for genotoxic/carcinogenic events. In this case-control study, blood/ sera samples of the COPD cases (n=32 identified spirometrically among the stone-crushing workers) and healthy controls (n=19) were assessed for 8-OHdG (DNA damage), glutathione and superoxide dismutase levels (oxidative stress) and genotyped for GSTT1, M1, P1 and MnSOD variants. Significant increase in oxidative damage and lung- function decline were observed as a function of some genotypes. Predictors of genetic damage included tGSH, SOD and GSTM1. A prognostic index score based on prognostic factors was developed revealing cases were at high- (53.12%), intermediate- (34.37%) or low- (12.50%) risk for progressive DNA damage. These aberrant findings imply workplace exposure. This study provides insight on exposure-effect relationship in workers at stone- crushing sites.

Oxidative stress-mediated apoptosis and genotoxicity induced by silver nanoparticles in freshwater snail Lymnea luteola L.

Silver is one of the most toxic metals to freshwater aquatic organisms. Limited efforts have been made to study apoptosis and genotoxic potential of silver nanoparticles (AgNPs) in freshwater snail Lymnea luteola L. (L. luteola). Therefore, the present investigation was aimed to study the induction of apoptosis and DNA damage by AgNPs in L. luteola. AgNPs showed molluscicidal activity against L. luteola and three concentrations of AgNPs were selected, the concentration I (4 μg/l), concentration II (12 μg/l), and the concentration III (24 μg/l). Induction of oxidative stress in snail hemolymph was observed by a decrease in reduced glutathione (GSH) and glutathione S-transferase (GST) levels at different concentration of AgNPs, and on the other hand, malondialdehyde (MDA) levels increased at lower concentrations but decreased in higher concentration of AgNPs. Catalase (CAT) activity was also decreased at lower concentrations and increased in higher concentration of AgNPs. Flow cytometry data showed that AgNPs exposed hemocyte cells promote apoptotic and necrotic-mediated cell death when AgNPs concentrations were 12 and 24 μg/l compared to control. DNA damage scores increased with the exposure levels of AgNPs, and dose- and time-dependent effects were observed. A significant positive correlation was observed among reactive oxygen species (ROS) generation, apoptosis, and DNA damage. The study suggests that ROS may be involved in inducing apoptosis and DNA damage in the AgNPs exposed hemocyte cells of L. luteola. This study demonstrates that AgNPs is lethal to freshwater snail L. luteola.

N-Acetylcysteine Supplementation Reduces Oxidative Stress and DNA Damage in Children with β-Thalassemia

There are several reports that increased oxidative stress and DNA damage were found in β-thalassemia major (β-TM) patients. In this study, we aimed to evaluate the effects of N-acetylcysteine (NAC) and vitamin E on total oxidative stress and DNA damage in children with β-TM. Seventy-five children with transfusion-dependent β-thalassemia (β-thal) were randomly chosen to receive 10 mg/kg/day of NAC or 10 IU/kg/day of vitamin E or no supplementation; 28 healthy controls were also included in the study. Serum total oxidant status (TOS) and total antioxidant capacity (TAC) were measured, oxidative stress index (OSI) was calculated, and mononuclear DNA damage was assessed by alkaline comet assay; they were determined before treatment and after 3 months of treatment. Total oxydent status, OSI, and DNA damage levels were significantly higher and TAC levels were significantly lower in the thalassemic children than in the healthy controls (p < 0.001). In both supplemented groups, mean TOS and OSI levels were decreased; TAC and pre transfusion hemoglobin (Hb) levels were significantly increased after 3 months (p ≤ 0.002). In the NAC group, DNA damage score decreased (p = 0.001). N-acetylcysteine and vitamin E may be effective in reducing serum oxidative stress and increase pre transfusion Hb levels in children with β-thal. N-acetylcysteine also can reduce DNA damage.

Genotoxic effects of the herbicide Roundup Transorb® and its active ingredient glyphosate on the fish Prochilodus lineatus

Roundup Transorb® (RT) is a glyphosate-based herbicide and despite its wide use around the world there are few studies comparing the effects of the active ingredient with the formulated product. In this context the purpose of this study was to compare the genotoxicity of the active ingredient glyphosate with the formulated product RT in order to clarify whether the active ingredient and the surfactant of the RT formula may exert toxic effects on the DNA molecule in juveniles of fish Prochilodus lineatus. Erythrocytes and gill cells of fish exposed to glyphosate and to RT showed DNA damage scores significantly higher than control animals. These results revealed that both glyphosate itself and RT were genotoxic to gill cells and erythrocytes of P. lineatus, suggesting that their use should be carefully monitored considering their potential impact on tropical aquatic biota.

Genotoxicity Evaluation of 1,2 Dichlorobenzene in the Indian Major Carp, Catla catla L. Using Alkaline Comet Assay

The genotoxic effect of 1,2 dichlorobenzene (1,2 DCB), a volatile organic compound in the Indian Major Carp, Catla catla L. was assessed using the alkaline comet assay in the gills and blood. Fish were exposed to various sub-lethal concentrations of 1,2 DCB in vivo. At 24h, DNA damage scores (expressed as arbitrary units) increased at 0.35 and 0.7mg/L whereas at 28days, there was a statistically significant increase in the DNA damage score at all the doses tested (0.175, 0.23, 0.35 and 0.7mg/L). When the DNA damage scores were considered in the blood samples, the trend was similar to that observed in the gills - significant increase at 0.35 and 0.7mg/L at 24h and at all doses at 28days. The results indicate that 1,2 DCB induces genotoxicity in the form of strand breaks in the DNA of fish as evidenced by the alkaline comet assay.

A study of DNA protective effect of orange juice supplementation

The potential acute genoprotective effect of orange juice supplementation was investigated. Six healthy subjects (aged 33 to 60 years; 3 women and 3 men) were asked to drink 400 mL of commercial orange juice, which contained 100 mg vitamin C and 40.8 g sugar. Venous blood (2 mL) was taken before and 2 h after ingestion (test trial). A week later, the subjects were asked to repeat the trial by drinking 400 mL water with 100 mg vitamin C and 40.8 g glucose (control trial). Lymphocytes isolated from blood samples underwent comet assay on the day of collection. Pre- and postingestion DNA damage scores were measured in both the test and control trials. Results showed that there was a significant decrease in DNA damage induced by hydrogen peroxide after 2 h of supplementation with orange juice, and no change in baseline DNA damage. There was no significant decrease in the DNA damage in lymphocytes in the control trial.

Genotoxicity profiles in exfoliated human mammary cells recovered from lactating mothers in Istanbul; relationship with demographic and dietary factors

We have investigated the presence of DNA damage in human mammary epithelial cells collected from healthy lactating mothers (age, 20–35 years) who were resident in the Istanbul area. Breast milk (10ml) was collected from 30 women between one and two weeks post-partum. Demographic information (parity, breast cancer, occupation, duration of residency in Istanbul, consumption of fish, beef and poultry) was also obtained. Milk samples were diluted 1:1 with RPMI 1640 medium and centrifuged to collect cells. The cells were re-suspended and cell viability was determined by use of 0.4% trypan blue. DNA damage was assessed by use of the comet assay (alkaline single-cell gel electrophoresis). Fifty cells per slide and two slides per sample were scored to evaluate DNA damage. The cells were visually classified into four categories on the basis of extent of migration: undamaged (UD), lightly damaged (LD), moderately damaged (MD) and highly damaged (HD). Total comet scores (TCS) were calculated as: 1× UD+2× LD+3× MD+4× HD. Exfoliated mammary cells of the donors showed high (TCS≥150a.u.), moderate and low DNA damage in 10 (33.3%), 8 (26.7%) and 12 (40%) mothers, respectively. There was no significant correlation between TCS for DNA damage and the duration of previous breastfeeding, parity or age. None of the mothers was vegetarian, smoker or on any medication. Meat and chicken consumption did not significantly correlate with the TCS values. Fish consumption was significantly correlated with TCS results (Spearman's rho=0.39, p<0.05). No significant correlation was found between the DNA-damage scores and the period of residency in Istanbul, but fish consumption increased as the duration of stay was longer (Spearman's rho=0.53, p<0.01). These findings suggest that the primary causes of differences in genotoxicity detected in lactating mothers in Istanbul may be of dietary origin. Our experience also confirms that sampling breast milk from lactating mothers provides a valuable and non-invasive tool to study DNA damage in mammary cells.

Genotoxicity Evaluation of Commercially Available Acid Red Dye by Comet Assay in Fish (Cyprinus Carpio)

Genotoxicity of commercially available acid red dye on fish was evaluated. Fish were exposed to various concentrations of the dye and gill processed for comet assay. Nucleoids were visually scored and categorized into various damage degrees. Significant increase (p < 0.05) in the percentage and distribution of damaged nucleoids was recorded in all dye-treated groups over control. DNA damage scores (AU) increased with exposure concentrations and dose-response was observed at higher doses. From the results it is concluded that commercially available acid red dye is potentially genotoxic to fish. The results are preliminary and further studies are warranted to acknowledge this effect. Keywords: acid red, commercial dyes, genotoxicity, comet assay.