Gursatej Gandhi

Genetic damage in mobile phone users: some preliminary findings

BACKGROUND: The impact of microwave (MW)/radio frequency radiation (RFR) on important biological parameters is probably more than a simply thermal one. Exposure to radio frequency (RF) signals generated by the use of cellular telephones have increased dramatically and reported to affect physiological, neurological, cognitive and behavioural changes and to induce, initiate and promote carcinogenesis. Genotoxicity of RFR has also been reported in various test systems after in vitro and/or in vivo exposure but none in mobile phone users. AIMS: In the present study, DNA and chromosomal damage investigations were carried out on the peripheral blood lymphocytes of individuals using mobile phones, being exposed to MW frequency ranging from 800 to 2000 MHz. METHODS: DNA damage was assessed using the single cell gel electrophoresis assay and aneugenic and clastogenic damage by the in vivo capillary blood micronucleus test (MNT) in a total of 24 mobile phone users. RESULTS: Mean comet tail length (26.76 ± 0.054 mm; 39.75% of cells damaged) in mobile phone users was highly significant from that in the control group. The in vivo capillary blood MNT also revealed highly significant (0.25) frequency of micronucleated (MNd) cells. CONCLUSIONS: These results highlight a correlation between mobile phone use (exposure to RFR) and genetic damage and require interim public health actions in the wake of widespread use of mobile telephony.

Cytogenetic Damage in Mobile Phone Users: Preliminary Data

Abstract Mobile telephones, sometimes called cellular (cell) phones or handies, are now an integral part of modern life. The mobile phone handsets are low-powered radiofrequency transmitters, emitting maximum powers in the range of 0.2 to 0.6 watts. Scientific concerns have increased sufficiently over the possible hazard to health from using cell phones. The reported adverse health effects include physiological, behavioural and cognitive changes as well as tumour formation and genetic damage. However findings are controversial and no consensus exists. Genotoxicity has been observed either in lower organisms or in vitro studies. The aim of the present study hence was to detect any cytogenetic damage in mobile phone users by analysing short term peripheral lymphocytes cultures for chromosomal aberrations and the buccal mucosal cells for micronuclei (aneugenicity and clastogenicity). The results revealed increased number of micronucleated buccal cells and cytological abnormalities in cultured lymphocytes indicating the genotoxic response from mobile phone use.

A cross-sectional case control study on genetic damage in individuals residing in the vicinity of a mobile phone base station

Abstract Mobile phone base stations facilitate good communication, but the continuously emitting radiations from these stations have raised health concerns. Hence in this study, genetic damage using the single cell gel electrophoresis (comet) assay was assessed in peripheral blood leukocytes of individuals residing in the vicinity of a mobile phone base station and comparing it to that in healthy controls. The power density in the area within 300 m from the base station exceeded the permissive limits and was significantly (p = 0.000) higher compared to the area from where control samples were collected. The study participants comprised 63 persons with residences near a mobile phone tower, and 28 healthy controls matched for gender, age, alcohol drinking and occupational sub-groups. Genetic damage parameters of DNA migration length, damage frequency (DF) and damage index were significantly (p = 0.000) elevated in the sample group compared to respective values in healthy controls. The female residents (n = 25) of the sample group had significantly (p = 0.004) elevated DF than the male residents (n = 38). The linear regression analysis further revealed daily mobile phone usage, location of residence and power density as significant predictors of genetic damage. The genetic damage evident in the participants of this study needs to be addressed against future disease-risk, which in addition to neurodegenerative disorders, may lead to cancer.

Elevated frequency of Micronuclei in uterine smears of cervix cancer patients

Abstract Epithelial scrapes of the cervix from patients with cervix cancer (n=30) and without the diseased condition (n=23) were processed for the micronucleus test. Statistical analysis of the data revealed significantly elevated frequency of micronucleated (MNd) cells in all the patients irrespective of the stage of cancer. The damage within the stage-types was however non-significant. Significantly elevated percent frequencies of MNd cells were also observed for pre-treated cervix cancer patients compared with the control data; for different ageat marriage groups; in aged patients; in the weaker socio-economic groups and in those with more child-bearing and/or total number of pregnancies; though within group differences were not always significant.

DNA and chromosomal damage in coronary artery disease patients

DNA and chromosomal damage in peripheral blood leukocytes of patients with coronary artery disease (CAD) were investigated by using the single cell gel electrophoresis assay /comet and cytokinesis- block micronucleus (CBMN) assays, respectively. The case-control study comprised patients with CAD (n = 46; average age 53.0 ± 1.27 y) undergoing treatment at local hospitals, and healthy age-and sex-matched controls (n = 19; average age 54.21 ± 0.91 y) from the general population. The results of the comet assay revealed that the mean values of DNA damage were significantly (p < 0.001) higher in CAD patients than in controls (Tail DNA% 11.55 ± 0.38 vs. 5.31 ± 0.44; Tail moment 6.17 ± 0.31 vs. 2.93 ± 0.21 AU; Olive tail moment 3.52 ± 0.23 vs. 1.25 ± 0.11 AU). The mean values of chromosomal damage were also significantly higher (p < 0.001) in CAD patients than in controls (Binucleated cells with MN- 28.15 ± 1.18 vs. 18.16 ± 2.59; micronuclei 29.52 ± 1.21 vs. 18.68 ± 2.64, respectively) while nuclear division index (1.48 ± 0.01 vs. 1.63 ± 0.01) was significantly higher (p < 0.001) in controls. The results of the present study indicate that coronary artery disease patients had increased levels of both, unrepaired (DNA) and repaired (chromosomal) genetic damage which may be a pathological consequence of the disease and/or the drug-treatment. This accumulation of DNA/chromosomal damage is of concern as it can lead to the development of cancer with increased chances of morbidity and mortality in the CAD patients.

Association of GSTT1 and GSTM1 gene polymorphisms with coronary artery disease in North Indian Punjabi population: a case-control study

Background Glutathione S-transferases are metabolic enzymes which are responsible for detoxification of endogenous (products of oxidative stress) as well as exogenous (drugs, pesticides, herbicides, environmental pollutants and carcinogens) products. Dysfunctional detoxification enzymes are responsible for the production of oxidative stress; a major contributor to the development of coronary artery disease (CAD). Objectives The present case-control study aimed to investigate the association of GSTT1 and GSTM1 gene polymorphisms with CAD. Methods In the present study, 200 patients diagnosed with CAD and 200 age, sex and population subgroup matched healthy controls were enrolled. The GSTT1 and GSTM1 gene polymorphisms were examined using multiplex PCR. Results The frequency of GSTT1 null genotype was significantly (p=0.038) lower in patients with CAD (6.00%) than in controls (12.50%). The GSTT1 null genotype showed protection against CAD (OR=0.45, 95% CI 0.22 to 0.92, p=0.028). The frequency of GSTM1 null genotype was significantly (p=0.004) higher in patients (31%) compared with controls (18%). The GSTM1 null genotype conferred twofold increased risk of developing CAD (OR=2.05, 95% CI 1.28 to 3.27, p=0.003). Conclusions The results concluded that the GSTT1 null genotype showed protection against CAD while the GSTM1 null genotype might be involved in the pathogenesis and development of CAD.

DNA Damage in Peripheral Blood Leukocytes of Physically Active Individuals as Measured by the Alkaline Single Cell Gel Electrophoresis Assay

DNA damage induced by physical activity and/or exercise has been reported under different conditions but not for individuals maintaining physical fitness by regular strenuous exercise. Therefore, we compared levels of DNA damage in blood leukocytes of 40 healthy individuals (35 males, 5 females) who regularly exercised in gymnasiums/health clubs and 15 healthy sedentary controls who had never exercised. The former group was selected (after informed consent) on the basis of how long they had been exercising on a regular basis as well as their exercise schedule and regimen. The length of time since starting a regular exercise regimen ranged from 2 months to 9 years, whereas the daily exercise duration ranged from 40 min to 3 hrs and warm‐up sessions ranged from none to 90 min. The length of DNA migration (44.66 ± 2.68 μm in males, 29.62 ± 1.69 μm in females) and the percentage of cells with tails (79.86 ±1.27% in males, 67.20 ± 0.96% in females) in peripheral blood leukocytes of physically active individuals were increased significantly (P < 0.001) with respect to corresponding values in control males and females (18.85 ± 1.79 μm, 23.37 ± 3.94 μm; 24.50 ± 1.98%, 33.00 ± 4.44%, respectively). Highly significant differences for DNA damage were also observed between physically active males and females. These observations, in the absence of any other exposures, indicate a correlation between strenuous exercise to keep fit and increased levels of DNA damage. This finding may have relevance in terms of the ageing process, with diseases associated with aging, and with carcinogenesis. Environ. Mal. Mutagen. 2009.

The Micronucleus Test in Urothelial Cells and Uterine Smears of Cervix Cancer Patients: A Comparison

Abstract Cytogenetic damage was assessed using the (MN) test in urothelial cells and cervix smears of local cervix cancer patients since the genetic end-point screening for micronuclei provides a measure of both, chromosome breakage and loss. The MN data were grouped for stage-types of cancer, age-groups, age-atmarriage, parity levels and socio-economic status. A comparison of the results obtained from both the tissues has revealed that the percent frequency of MNd cells was elevated in urothelial cells except when the variable for age-groups of the patients was compared. If validated, the MN assay in urothelial cells may prove useful for screening programmes for cervix cancer as besides scoring effectively for cytogenetic damage, it utilizes a non-invasive process of sample collection.

Exercise-Induced Genetic Damage: A Review

Abstract Physical activity improves the quality of life and well being in healthy persons and has been demonstrated to have beneficial effect on quality of life during and after therapy in cancer patients. Considerable evidence on the other front has shown an association between physical activity and genetic damage and also implied a possible role of physical activity on cancer incidence. Diverse biologic mechanisms have sought to explain the complex relationship between energy balance, physical activity and genetic damage. Primary and secondary reactions have been implicated. These include free radical damage, immune dysfunction, mechanical injury, sex hormones, growth factors, cytokines, etc. Alterations in pro-and antiapoptotic proteins during long-term physical activity can possibly explain why exercise training relates to inconsistence in cancer causing. Future research is needed in this direction for possible intervention trials. The value of antioxidant supplementation for attenuating post-exercise tissue damage cannot be undermined though more conclusive studies are required for exact recommendations.

Assessment of DNA Damage in Leukocytes of Patients With Coronary Artery Disease by Comet Assay

DNA damage in the peripheral blood leukocytes (PBL) of patients with coronary artery disease (CAD) was investigated using the sensitive alkaline single cell gel electrophoresis (SCGE)/comet assay.This case-control study consisted of CAD patients (n = 200; mean age, 59.04 ± 0.75 years) undergoing treatment at local hospitals and age-, sex-, and ethnicity-matched healthy controls (n = 200; mean age, 57.88 ± 0.96 years) from the general population.CAD patients had significantly (P < 0.001) increased DNA damage (tail DNA percent (T-DNA %) 22.45 ± 0.50 versus 5.81 ± 0.28; tail moment (TM) 89.35 ± 3.16 versus 9.98 ± 0.69; Olive tail moment (OTM) 60.50 ± 1.79 versus 10.94 ± 0.63; damage frequency (DF) 91.12 ± 0.93 versus 41.78 ± 2.04, damage index (DI) 173.68 ± 3.36 versus 48.53 ± 2.59) compared to controls. Patients with acute myocardial infarction (AMI) showed significantly higher DNA damage than patients with unstable angina (UA) (T-DNA % 24.05 ± 0.87 versus 21.06 ± 0.90; TM 100.02 ± 6.19 versus 81.61 ± 5.84; OTM 66.19 ± 3.20 versus 56.47 ± 3.33; DF 94.02 ± 0.84 versus 91.10 ± 1.16, DI 184.13 ± 5.33 versus 166.42 ± 5.89). Moreover, DNA damage was found to be significantly (P < 0.05) elevated in patients receiving ecosprin, ramipril, and metoprolol therapy compared to aspirin and nitrocontin.The increased DNA damage in CAD patients may be the consequence of disease and/or drug therapy. These observations are of concern because unrepaired DNA can lead to malignancy, and the likelihood of increasing mortality and morbidity rates in CAD patients.