Assessment of DNA Damage in Chick Embryo Brains Exposed to 2G and 3G Cell Phone Radiation using Alkaline Comet Assay Technique

Introduction: The cellular phones/mobile phones have emerged as the fastest growing man-made phenomenon ever discovered in the history. Controversies still exist among the scientific community regarding the ill-effects of Radiofrequency Radiation (RFR) exposure from cell phones on biological tissues. The present study will provide an insight into the basic mechanisms by which RF fields interact with developing brain in an embryo. Aim: To assess the possible Deoxyribonucleic Acid (DNA) damage in developing brain of chick embryo following chronic exposure to Ultra-High Frequency/Radiofrequency Radiation (UHF/RFR) emitted from 2G and 3G cell phone. Materials and Methods: Fertilised hen eggs were divided into three groups. Experimental Group A (exposed to 2G radiation, 24 eggs), Experimental Group B (exposed to 3G radiation, 24 eggs) and Group C sham exposed control group (24 eggs). After the completion of scheduled duration of exposure (72 minutes per day), the chick embryos were sacrificed from 9th-12th day and the brains were dissected out. The chick embryo brains were then subjected to alkaline comet assay technique to assess the DNA damage. The results were statistically compared using one-way Analysis of Variance (ANOVA). Results: In the present study, the exposure of chick embryo brains to 2G and 3G cell phone radiation caused increased mean comet length (p<0.001), mean tail length (p<0.001), mean percentage of DNA in the tail (p<0.001) and mean tail moment (p<0.01) suggestive of increased DNA damage. Conclusion: The present study concludes that the RFR exposure caused significant increase in DNA damage in developing brain of chick embryos with changes more pronounced in 3G exposure group.

Biomonitoring findings for occupational lead exposure in battery and ceramic tile workers using biochemical markers, alkaline comet assay, and micronucleus test coupled with fluorescence in situ hybridisation

Manufacture of lead-containing products has long been associated with various health risks. To get an insight into the related genotoxic risks, we conducted a biomonitoring study in 50 exposed workers and 48 matched controls using a battery of endpoints that sensitively detect the extent of genome instability in peripheral blood lymphocytes. The levels of primary DNA damage were estimated with the alkaline comet assay, while cytogenetic abnormalities were determined with the cytokinesis-block micronucleus (CBMN) cytome assay. Additionally, CBMN slides of 20 exposed and 16 control participants were subjected to fluorescence in situ hybridisation (FISH), coupled with pancentromeric probes to establish the incidence of centromere-positive micronuclei, nuclear buds, and nucleoplasmic bridges. Blood lead levels (B-Pb) were measured with atomic absorption spectrometry. To further characterise cumulative effects of occupational exposure, we measured erythrocyte protoporphyrin (EP) concentrations and delta-aminolevulinic acid dehydratase (ALAD) activity in blood. We also assessed the influence of serum folate (S-folate) and vitamin B12 (S-B12) on genome stability. Compared to controls, occupationally exposed workers demonstrated significantly higher B-Pb (298.36±162.07 vs 41.58±23.02), MN frequency (18.71±11.06 vs 8.98±7.50), centromere positive MN (C+ MN) (8.15±1.8 vs 3.69±0.47), and centromere negative MN (C- MN) (14.55±1.80 vs 4.56±0.89). Exposed women had significantly higher comet tail intensity (TI) and length (TL) than control women. Furthermore, workers showed a positive correlation between age and nuclear buds and MN, between MN and years of exposure, and between S-B12 levels and TI and ALAD activity, while a negative correlation was found between TI and B-Pb. These findings suggest that occupational settings in the manufacture of lead-containing products pose significant genotoxic risks, which calls for developing more effective work safety programmes, including periodical monitoring of B-Pb and genetic endpoints.