Chromosome Damage In Lymphocytes Research Articles

Morphological abnormalities of peripheral blood cells among patients with COVID-19 disease

PurposeThe hematological changes in COVID-19 patients continue to receive great attention, especially in the field of public health. To our knowledge, coronavirus disease may be identified based on the severity of illness, and the study of peripheral blood smears may offer important information to facilitate the identification. Thus, we evaluated the morphological abnormalities (atypical and immature lymphocytes, lymphocytes with micronuclei, various nuclear abnormalities among erythrocytes) and quantitative changes in peripheral blood cells among 48 individuals with COVID-19 disease. MethodsThe present study is a retrospective analysis of 48 individuals, including 24 hospitalized patients diagnosed with COVID-19 disease. The blood smears of all patients were subjected to a hematological examination to identify various morphological abnormalities in white and red blood cells. In addition, a micronucleus test was conducted to assess the incidence of chromosomal damage in lymphocytes. Furthermore, the complete blood count (CBC) was performed to evaluate changes in peripheral blood cells, particularly the differential total leukocyte count, which could indicate the immune response against viral infection in COVID-19 patients. ResultsThe findings of the hematological study conducted on patients diagnosed with COVID-19 disease revealed neutrophilia, eosinophilia, mild monocytosis, decreased hematocrit level, elevated erythrocyte sedimentation rate (ESR), and immature leukocytes. It was observed that patients who were infected with coronavirus demonstrated mild thrombocytopenia. Furthermore, the micronucleus test indicated the presence of immature cells with micronuclei among lymphocytes and numerous nuclear abnormalities in red blood cells. These results help to shed light on the hematological changes that occur in COVID-19 patients, and could potentially contribute to the development of more effective treatments for the disease. ConclusionsThe examination of complete blood counts (CBCs) in conjunction with peripheral blood smears offers a potential means of identifying the impact of SARS-CoV-2 infection on the hematopoietic and immune systems, thereby providing early indications of inflammation. Based on a study, it has been suggested that SARS-CoV-2 may affect red and white blood cells causing morphological alterations thereby establishing a corresponding relationship with disease severity.

Influence of Body Mass Index and Duration of Disease on Chromosome Damage in Lymphocytes of Patients with Diabetes.

It is well-established that patients with diabetes mellitus (DM) have a higher incidence of several types of cancer. The precise mechanisms of this association are still unknown, but obesity and chronic inflammation-induced reactive oxygen species (ROS) are thought to be the main risk factors. ROS may produce different DNA damage, which could eventually lead to cancer. The main objective of this study was to evaluate the relation of chromosome aberrations (CA) with disease status, demographics, and clinical parameters in 33 subjects with type 1 DM (T1DM), 22 subjects with type 2 DM (T2DM), and 21 controls. CAs were analyzed in cultured peripheral blood lymphocytes and subdivided into chromatid (CTA)- and chromosome (CSA)-type aberrations. Compared with controls, higher levels of CTAs and CSAs were observed in T1DM (p = 0.0053 and p = 0.0203, respectively) and T2DM (p = 0.0133 and p = 0.00002, respectively). While there was no difference in CTAs between T1DM and T2DM, CSAs were higher in T2DM (p = 0.0173). A significant positive association between CTAs and disease duration (rs = 0.2938, p = 0.0099) and between CSAs and disease duration (rs = 0.4306, p = 0.0001), age (rs = 0.3932, p = 0.0004), and body mass index (BMI) (rs = 0.3502, p = 0.0019) was revealed. After multiple regression analysis, duration of disease remained significant for CTA, CSA, and CAs (p = 0.0042, p = 0.00003, and p = 0.00002, respectively). For CSA, BMI and the use of statins were the other important confounding variables (p = 0.0105 and p = 0.0763). Thus, this study demonstrated that both T1DM and T2DM patients had a higher number of all types of aberrations than controls, which increases with the prolonged disease duration. Higher BMI was associated with a higher frequency of CSA. The use of statins might be beneficial for reducing chromosome damage, but further investigations are needed to confirm this association.

Different chromosome damage in lymphocytes of newly diagnosed gastrointestinal and breast cancer patients.

Structural chromosome aberrations are a predictive biomarker of cancer risk. Conventional chromosome analysis widely used for these purposes detects unstable chromosome aberrations that are eliminated during cell division. Stable aberrations that may persist in the body and tend to accumulate during a lifetime can be detected by fluorescence in situ hybridization (FISH). The aim of the study was to investigate the level of chromosome damage in newly diagnosed cancer patients and control subjects by FISH. Both groups of untreated cancer patients had increased frequency of aberrant cells. However, chromosome damage affected different cytogenetic endpoints. Stable translocations and cells with complex rearrangements were elevated in breast cancer patients whereas unstable chromosome aberrations (dicentric chromosomes and acentric fragments) were elevated in gastrointestinal cancer patients. These associations observed in nonsmokers were typically not pronounced in smokers (with the exception of dicentric chromosomes in gastrointestinal patients). Exposure to tobacco smoke increased aberrations in healthy controls but not in the cancer patients. Our study suggests an association between cancer and stable chromosomal rearrangements in breast cancer patients. Unstable aberrations elevated in gastrointestinal cancer patients may be at least partly ascribed to the exposure to diagnostic X-rays.

Decreased Chromosomal Damage in Lymphocytes of Obese Patients After Bariatric Surgery

The number of bariatric surgeries being performed worldwide has markedly risen. While the improvement in obesity-associated comorbidities after bariatric surgery is well-established, very little is known about its impact on cancer risk. The peripheral lymphocyte micronucleus test is a widely used method for the monitoring of chromosomal damage levels in vivo, and micronucleus frequency positively correlates with cancer risk. Therefore, the aim of this study was to compare the micronucleus frequency before and after bariatric surgery in obese subjects. Peripheral blood mononuclear cells were collected from 45 obese subjects before and at two time-points after bariatric surgery (6 and 12 months) to assess spontaneous micronucleus frequency. Consistent with the increased cancer risk previously shown, bariatric surgery-induced weight loss led to a significant reduction in lymphocyte micronucleus frequency after 12 months. Interestingly, comorbidities such as type 2 diabetes mellitus and metabolic syndrome further seemed to have an impact on the lymphocyte micronucleus frequency. Our findings may indicate a successful reduction of cancer risk in patients following weight loss caused by bariatric surgery.

Micronucleus frequency and content in healthy relatives of cancer patients

Objective: To compare chromosomal damage in lymphocytes of individuals who did or did not report first-degree relatives with cancer.Materials and methods: Cases and controls (68 each) were matched for sex, age and radon exposure. Chromosomal damage was quantified as frequency of micronucleus-containing cells and proportion of centromere-free micronuclei.Results: Individuals not reporting cancer in their families showed lower values of both the frequency of micronucleus-containing cells (n.s.) and the proportion of centromere-free micronuclei (p < 0.05) in some subgroups, but not in all.Conclusion: The chromosomal damage observed may be due to inheritable genomic instability, but environmental influences cannot be excluded.

Evaluation of Genetic Damage in Tobacco Chewing Population by In-vitro SCE Assay: a Review from Coastal Andhra Population

Background/Objectives: To understand the genotoxicity and cytotoxicity potentials in tobacco-chewing habitues from coastal Andhra Population. Place and Duration of Study: Translational Research Institute of Molecular Sciences, between October 2013 to October 2014. Methods/Statistical Analysis: Present study was carried out using 35 individuals (28 men, 7 women; age range 25-56 years) who are having a habit of chewing tobacco from 5-20 years were tested along with 35 controls with same age group. Samples were cultured and stained with Hoechst 3325. Scored chromosomal abnormalities, SCE’s, CPK and MI using statistical evaluations. Results/Findings: In this study we have scored the numerical and structural abnormalities, Mitotic Index (MI), Cell Proliferation Kinetics (CPK) and Sister Chromatid Exchanges (SCE’s) of the presented samples have been calculated. Although significant numerical aberration observed, structural abnormalities were notably seen in a few cases. When compared with controls tobacco-chewing habitues does increase induced significant mito depression. Our data reveals that samples CPK values were remarkably decreased when compared to control value. Conclusion/Application: The demonstration of chromosomal damage in lymphocytes from tobacco chewing habitues strongly indicates that tobacco should be categorized as a human carcinogen and major risk factor for oral, throat and pharynx cancers.

Translocations in Spleen Cells from Adult Mice Irradiated as Fetuses are Infrequent, but Often Clonal in Nature

We previously reported that mouse fetuses or neonates exposed to 2 Gy of X rays showed an unexpectedly low incidence of chromosome damage in lymphocytes, bone marrow, and spleen cells when the mice were subsequently examined at 20 weeks of age. However, cells bearing translocations were occasionally observed that, on the basis of 2-color whole chromosome painting appeared to be clonal descendants. Unfortunately, this approach typically did not permit unequivocal confirmation of their clonality. To overcome this problem, multi-color FISH (mFISH) was employed, which assigns all 21 individual chromosome types of the mouse a unique color. After mFISH analyses of the same cell samples studied previously, it was confirmed that spleen cells of 20-week-old mice irradiated either as 15.5-day fetuses or as 3- to 4-day-old neonates showed translocation frequencies close to zero. Translocations previously suspected as being clonal in nature were confirmed as such by mFISH, which also revealed the presence of an additional clone not previously detected or suspected. Since no evidence of clonality was observed in the irradiated mother, we concluded that in both fetuses and neonates, there exists a small fraction of stem cells that are distinct from the bulk of the stem cell compartment in terms of their ability to acquire and transmit radiation-induced chromosome damage through clonal expansion.

A Verification of Treatment Protocol in Fractionated Radiotherapy by Biological Dosimetry

In radiation therapy of cancer, any possible mistakes that may occur in prescribed tumour dose calculation and/ or in treatment set up could also be checked by the biological dosimetry. In order to verify this, 20 patients having pelvic area tumours with no prescribed chemotherapy were selected. Their peripheral blood samples were collected before starting fractionated radiotherapy and at some definite time during treatment. Equivalent whole body doses (EWBD) were calculated from patient’s weights, irradiated volumes and total tumor doses given until the date of blood sample collection during treatment. Each patient’s EWBD was given in vitro to blood samples that were collected before starting radiotherapy. Radiation induced chromosome damage in lymphocytes were measured by micronucleus (MN) induction. The relationship between the micronucleus frequencies (MN/BN) scored during therapy ( in vivo ) and the micronucleus frequencies scored after the application of in vitro EWBD was investigated. MN/BN rates scored following in vitro application of EWBD differed between 0.195 and 0.540, whereas MN/BN rates obtained during radiotherapy equivalent to EWBD differed between 0.213 and 0.625. It was shown that there was no significant difference (p=0.653) between the MN scores following in vitro applied EWBD and MN scores obtained in vivo . The existence of this correlation has confirmed the correct application of fractionated radiotherapy and treatment setup for the patients.

Relationship between urinary 1-hydroxypyrene level and peripheral blood lymphocyte chromosomal damage among coke oven workers

To investigate the relationship between the urinary 1-hydroxypyrene level and cytokinesis-block micronucleus in peripheral blood lymphocyte in coke oven workers. One hundred and fifty-eight workers from a coke plant and 158 referents without occupational PAHs exposure were recruited in this study. Urnary level of 1-hydroxypyrene was measured by alkaline hydrolysis combined with high performance liquid chromatography as an internal exposure dose, and the chromosomal damage of peripheral blood lymphocyte were evaluated with cytokinesis-block micronucleus (CBMN) method. Personal information including occupational history, age, sex, smoking and alcohol drinking, was collected by questionnaire. The lymphocyte chromosomal damage level expressed as frequency of CBMN in coke oven workers was significantly higher than that of controls (3.32 ± 2.90 vs 0.57 ± 0.88, P < 0.01) after adjusting for sex, age, smoking and alcohol drinking, and correlation between urinary 1-hydroxypyrene concentrations and frequency of CBMN was found (Spearman Partial correlation coefficient = 0.28, P < 0.05) in coke oven workers. Three hundreds and sixteen subjects were divided into three groups by their urine 1-hydroxypyrene level (expressed as 0.11 ∼ 0.70, 0.71 ∼ 4.09 and 4.10 ∼ 24.74 µmol/mol Cr). After adjusting for age, sex, smoking and alcohol drinking by multiple nonparametric analysis of covariance, the frequency of CBMN in the groups of 0.71 ∼ 4.09 and 4.10 ∼ 24.74 µmol/mol C were 1.89 ± 2.37 and 3.29 ± 2.36, significantly higher than that in the group of 0 ∼ 0.70 µmol/mol Cr (0.56 ± 0.89). Under present PAHs exposure levels, the Cytokinesis-block micronucleus test could detect PAHs-induced genotoxicity in coke oven workers.

Chromosomal damage in peripheral blood lymphocytes of newly diagnosed cancer patients and healthy controls

The majority of human cancers arise from cells unable to maintain genomic stability. Recent prospective studies indicated that enhanced chromosomal aberrations (CAs) frequencies are predictive of gastrointestinal and lung cancers. However, studies on incident cancer patients are lacking; thus, we investigated chromosomal damage in newly diagnosed cancer patients and healthy individuals. We analyzed chromosomal damage in peripheral blood lymphocytes in a group of 300 incident cancer patients (with different malignancies) in comparison with 300 healthy controls. The frequencies of aberrant cells (ACs) and CAs were significantly higher in patients (2.38 +/- 1.56 and 2.53 +/- 1.69, respectively) as compared with controls (1.81 +/- 1.31 and 1.94 +/- 1.47, respectively, P < 0.01). The percentual difference in chromatid-type aberrations (CTAs) between patients and controls was moderately significant (1.37 +/- 1.20 and 1.11 +/- 0.99, respectively, P <or= 0.05), whereas the difference in chromosome-type aberrations (CSAs) was stronger (1.16 +/- 1.24 versus 0.83 +/- 1.12, P < 0.01). Using binomial logistic regression, the estimated odds ratios and 95% confidence interval for ACs were 1.33 (1.18-1.49), P < 0.01; for CAs, 1.27 (1.14-1.41), P < 0.01; for CTA 1.24 (1.07-1.44), P < 0.01 and for CSA, 1.27 (1.10-1.47), P < 0.01. By stratifying patients for distinct neoplasia, markers of chromosomal damage were significantly enhanced in patients with breast, prostate and head/neck cancers, whereas no effect was recorded in patients affected by gastrointestinal cancers. The present study shows for the first time evidence of increased chromosomal damage in lymphocytes of incident cancer patients compared with healthy controls. The effects were observed in different cancer types but as the number of patients was relatively small, further studies are warranted.

Relationship between chromosome damage in lymphocytes and oxidative stress in patients with alcoholic liver disease

Relationship between chromosome damage in lymphocytes and oxidative stress in patients with alcoholic liver disease

Spontaneous and bleomycin‐induced chromosome damage in non cancer thyroid patients

Presence of chromosome damage in lymphocytes of patients affected by several diseases, including cancer, was detected by the micronucleus (MN) assay. Individual susceptibility to DNA damage, considered as a risk factor for cancer, can be also evaluated using the bleomycin (BLM) sensitivity test. We aimed to evaluate spontaneous or BLM-induced MN frequencies in autoimmune (AI, n = 19) and non autoimmune (NAI, n = 11) thyroid patients, not receiving (131)I radiometabolic therapy with respect to a control group of 18 healthy subjects. According to thyroid function, patients were also divided into hypothyroid (n = 10), euthyroid (n = 13) or hyperthyroid (n = 7) subjects. Spontaneous MN frequencies of AI and NAI patients did not differ from those of controls. Hypothyroid patients had more elevated MN basal levels (9.00 + or - 1.71 per thousand) than hyperthyroid (3.75 + or - 1.17 per thousand, P < 0.05) and euthyroid (5.38 + or - 0.97 per thousand, P < 0.01) patients or healthy subjects (4.17 + or - 0.63 per thousand, P < 0.01). In particular, the hypothyroid AI group showed the highest value (9.79 + or - 2.26 per thousand, P < 0.01). All thyroid patients responded differently to BLM than controls (39.90 + or - 2.48 per thousand vs. 31.08 + or - 2.51 per thousand, P = 0.0377). The NAI group had BLM-induced MN levels (45.00 + or - 2.56 per thousand) significantly higher (P = 0.0215) than AI patients (36.95 + or - 3.49 per thousand) or healthy subjects (31.08 + or - 2.51 per thousand). No significant difference was seen when patients were stratified according to autoimmunity. We report that hypothyroid patients exhibit a moderate increase in the level of spontaneous genome damage, and that AI thyroid patients resulted to be less sensitive than NAI patients to the mutagen sensitivity test. In prospective, it may be of interest to reinvestigate hypothyroid patients when correction of their dysfunction is achieved.

Spontaneous and radiation-induced chromosomal instability and persistence of chromosome aberrations after radiotherapy in lymphocytes from prostate cancer patients

The aim of the study was to compare the spontaneous and ex vivo radiation-induced chromosomal damage in lymphocytes of untreated prostate cancer patients and age-matched healthy donors, and to evaluate the chromosomal damage, induced by radiotherapy, and its persistence. Blood samples from 102 prostate cancer patients were obtained before radiotherapy to investigate the excess acentric fragments and dicentric chromosomes. In addition, in a subgroup of ten patients, simple exchanges in chromosomes 2 and 4 were evaluated by fluorescent in situ hybridization (FISH), before the onset of therapy, in the middle and at the end of therapy, and 1 year later. Data were compared to blood samples from ten age-matched healthy donors. We found that spontaneous yields of acentric chromosome fragments and simple exchanges were significantly increased in lymphocytes of patients before onset of therapy, indicating chromosomal instability in these patients. Ex vivo radiation-induced aberrations were not significantly increased, indicating proficient repair of radiation-induced DNA double-strand breaks in lymphocytes of these patients. As expected, the yields of dicentric and acentric chromosomes, and the partial yields of simple exchanges, were increased after the onset of therapy. Surprisingly, yields after 1 year were comparable to those directly after radiotherapy, indicating persistence of chromosomal instability over this time. Our results indicate that prostate cancer patients are characterized by increased spontaneous chromosomal instability. This instability seems to result from defects other than a deficient repair of radiation-induced DNA double-strand breaks. Radiotherapy-induced chromosomal damage persists 1 year after treatment.

Micronucleus-centromere assay and DNA repair gene polymorphism in lymphocytes of industrial radiographers

The micronucleus-centromere assay using a pan-centromeric probe was used to assess chromosomal damage in lymphocytes of 47 industrial radiographers occupationally exposed to low dose ionizing radiation and 47 controls. The influence of genotype of DNA repair genes ( XRCC1 399 , XRCC3 241 and XPD 751 ) on micronuclei (MN) frequency was also investigated. Centromere negative micronuclei (MNC−) frequency was significantly higher in radiographers than in controls, whereas similar centromere positive micronuclei (MNC+) frequency was observed in both groups. Poisson regression analyses revealed that the MNC− frequency was significantly associated with radiation occupational exposure and with cumulative-radiation doses in radiographers, after adjusting for confounding variables such as age, smoking, alcohol intake and genotypes. Compared to homozygous wild-type subjects, MNC− frequency in radiographers with variant XRCC3 genotype was significantly higher using univariate analysis. There were no differences in MNC− or MNC+ frequencies by genotype in controls. In conclusion, scoring of MNC− is a useful cytogenetic biomonitoring method for radiographers. Polymorphisms in XRCC3 might contribute to the increased genetic damage in individuals occupationally exposed to chronic ionizing radiation.

No Chromosomal Damage Seen From ADHD Medications

Back to table of contents Previous article Next article Clinical & Research NewsFull AccessNo Chromosomal Damage Seen From ADHD MedicationsJun YanJun YanSearch for more papers by this authorPublished Online:2 Jan 2009https://doi.org/10.1176/pn.44.1.0018aStimulants commonly used to treat attention-deficit/hyperactivity disorder (ADHD), specifically methylphenidate and amphetamine, do not cause chromosomal damages in circulating white blood cells, a study in the December 2008 Journal of the American Academy of Child and Adolescent Psychiatry finds.A study published in the December 18, 2005, Cancer Letters presented evidence of an increased frequency of three types of chromosomal damage in peripheral lymphocytes in 12 children after they had taken methylphenidate for three months. These types of chromosomal damage indicate DNA damage and structural changes to chromosomes and are associated with an increased risk of cancer.Since this alarming finding, several smaller human, in vitro, and animal studies were published that failed to replicate the stimulant-associated chromosomal damage seen in the original study.The new study was conducted with a methodology similar to the original study, but expanded the number of subjects and included mixed amphetamine salts (MAS) in addition to methylphenidate. Sixty-three children aged 6 to 12 with a DSM-IV diagnosis of ADHD were randomly assigned to open-label treatment with either methylphenidate or MAS for three months. None of them had taken stimulants before.The researchers found no significant increase from baseline to the end of the three-month treatment in any of the types of chromosomal damage reported in the previous study in either patients who took methylphenidate (n=25) or those who took MAS (n=22). In addition to these 47 subjects, 14 discontinued study participation prematurely for various reasons, and two were switched to different medications by their physicians and completed three months of treatment. No significant association between treatment and chromosomal damage was found in these individuals.The researchers examined the participants' blood samples, taken before and after the three months of stimulant treatment, for any chromosomal damage in lymphocytes. The percentages of cells with the damage at both time points as well as between the methylphenidate and the MAS groups were compared. No significant difference was seen between the two groups.The study was conducted at the Duke University Medical Center by Kristine Witt, M.S., and colleagues affiliated with the National Institute of Child Health and Human Development (NICHD) and the National Toxicology Program of the National Institute of Environmental Health Sciences (NIEHS). NICHD and NIEHS, both divisions of the National Institutes of Health, provided funding for the study.“These results add to the accumulating evidence that therapeutic levels of methylphenidate do not induce cytogenetic damage in humans,... and amphetamine-based products do not pose a risk for cytogenetic damage in children,” the authors concluded.An abstract of “Methylphenidate and Amphetamine Do Not Induce Cytogenetic Damage in Lymphocytes of Children With ADHD” is posted at<www.jaacap.com/pt/re/jaacap/abstract.00004583-200812000-00006.htm>.▪ ISSUES NewArchived

Sensitivity to cisplatin-induced mutations and elevated chromosomal aberrations in lymphocytes from sickle cell disease patients

Sickle cell disease (SCD) is an inherited disorder caused by a single nucleotide substitution in the beta-globin gene. The clinical heterogeneity observed in SCD patients has been attributed to environmental and genetic factors. The patients are subjected to increased oxidative stress, particularly during vaso-occlusive crises and acute chest pain. Another possible cause of oxidative stress in SCD is the high concentration of iron in the patients' plasma. The increase in oxidative stress could be a relevant risk factor for mutagenesis and carcinogenesis. Studies on the frequency of basal chromosomal aberrations in cultured lymphocytes from SCD patients have not been reported so far. In order to contribute to the understanding of the role of the different biomarkers and their relationship with the extremely variable clinical manifestation of SCD, we investigated the frequency of chromosome damage in peripheral lymphocytes from sickle cells patients and healthy controls. We found an increased frequency of chromosome damage and percentage of aberrant metaphases in these patients when compared with control subjects, even at basal values (p<0.05). In the cytogenetic sensitivity assay, the results showed that these patients presented a marked decrease in the mitotic index values compared with healthy controls. Cisplatin-induced chromosomal damage in lymphocytes from these patients was significantly higher than the frequency measured in healthy controls. The results obtained in the present study showed that more investigations are needed in order to elucidate the susceptibility to genomic instability of SCD patients.

Acute chromosomal DNA damage after radiation exposure

We read the article by Andreassi et al. 1 dealing with the impact of radiation exposure on acute chromosomal DNA damage in human lymphocytes with great interest. The authors reported significantly increased chromosomal damage in lymphocytes by revealing increased percent of micronucleus in samples of second and 24th hours after radiation exposure in invasive cardiovascular procedures compared to baseline levels. In our …

Risk assessment of welders using analysis of eight metals by ICP-MS in blood and urine and DNA damage evaluation by the comet and micronucleus assays; influence of XRCC1 and XRCC3 polymorphisms

The aims of the present study were to assess the occupational risk of welders using analysis of metals in biological fluids, DNA damage evaluation by complementary genotoxic endpoints and the incidence of polymorphisms in DNA repair genes. A biomonitoring study was conducted that included biometrology (blood and urinary concentrations of aluminium, cadmium, chromium, cobalt, lead, manganese, nickel, zinc by ICP-MS), comet and cytokinesis-block micronucleus assays in peripheral lymphocytes and genetic polymorphisms of XRCC1 (p.Arg399Gln) and XRCC3 (p.Thr241Met). This study included 60 male welders divided into two groups: group 1 working without any collective protection device and group 2 equipped with smoke extraction systems. A control group (n = 30) was also included in the study. Higher chromium, lead and nickel blood and urinary concentrations were detected in the two groups of welders compared to controls. Statistically differences between welders of group 1 and group 2 were found for blood concentration of cobalt and urinary concentrations of aluminium, chromium, lead and nickel. The alkaline comet assay revealed that welders had a significant increase of OTMchi2 distribution at the end of a work week compared to the beginning; a significant induction of DNA strand breaks at the end of the week was observed in 20 welders out of 30. The cytokinesis-block micronucleus assay showed that welders of group 1 had a higher frequency of chromosomal damage than controls. The XRCC1 variant allele coding Gln amino acid at position 399 was found to be associated with a higher number of DNA breaks as revealed by the comet assay. Increased metal concentrations in biological fluids, DNA breaks and chromosomal damage in lymphocytes emphasized the need to develop safety programmes for welders.

Chromosomal aberrations in arsenic-exposed human populations: a review with special reference to a comprehensive study in West Bengal, India

For centuries arsenic has played an important role in science, technology, and medicine. Arsenic for its environmental pervasiveness has gained unexpected entrance to the human body through food, water and air, thereby posing a great threat to public health due to its toxic effect and carcinogenicity. Thus, in modern scenario arsenic is synonymous with “toxic” and is documented as a paradoxical human carcinogen, although its mechanism of induction of neoplasia remains elusive. To assess the risk from environmental and occupational exposure of arsenic, in vivo cytogenetic assays have been conducted in arseniasis-endemic areas of the world using chromosomal aberrations (CA) and sister chromatid exchanges (SCE) as biomarkers in peripheral blood lymphocytes. The primary aim of this report is to critically review and update the existing in vivo cytogenetic studies performed on arsenic-exposed populations around the world and compare the results on CA and SCE from our own study, conducted in arsenic-endemic villages of North 24 Parganas (district) of West Bengal, India from 1999 to 2003. Based on a structured questionnaire, 165 symptomatic (having arsenic induced skin lesions) subjects were selected as the exposed cases consuming water having a mean arsenic content of 214.96 µg/l. For comparison 155 age-sex matched control subjects from an unaffected district (Midnapur) of West Bengal were recruited. Similar to other arsenic exposed populations our population also showed a significant difference (P < 0.01) in the frequencies of CA and SCE between the cases and control group. Presence of substantial chromosome damage in lymphocytes in the exposed population predicts an increased future carcinogenic risk by this metalloid.

A Preliminary Study to Assess Possible Chromosomal Damage Among Users of Digital Mobile Phones

In a preliminary study to examine possible lymphocyte chromosomal damage, we have tested two cytogenetic endpoints, namely, chromosomal aberrations (CA) and sister chromatid exchange frequencies (SCE), in 24 mobile phone users (12 nonsmoker–nonalcoholic subjects and 12 smoker–alcoholics), who used digital mobile phones for at least 2 years, employing Gaussian Minimum Shift Keying modulations with uplink frequencies at 935–960 MHz. and downlinks at 890–915 MHz. For comparison, the control study group included another 24 individuals, matched according to their age, sex, drinking and smoking habits, as well as similar health status, working habits, and professional careers; but did not use mobile phones. Blood samples of 12 mobile users (6 smoker–alcoholic and 6 nonsmoker–nonalcoholic) and 12 controls (identical to mobile users in every respect) were further treated with a known mutagen Mitomycin‐C (MMC) to find out comutagenic/synergistic effect. A complete blood picture for each individual was assessed with an automatic particle cell counter.There was a significant increase (P < 0.05) in dicentric chromosomes among mobile users who were smoker–alcoholic as compared to nonsmoker–nonalcoholic; the same held true for controls of both types. After MMC treatment, there was a significant increase in dicentrics (P < 0.05) and ring chromosomes (P < 0.001) in both smoker–alcoholic and nonsmoker–nonalcoholic mobile users when compared with the controls. Although SCEs showed a significant increase among mobile users, no change in cell cycle progression was noted. The hematological picture showed only minor variations between mobile users and controls.