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Total 84 patients were included in this study out of which 50 were males and 34 were females. During overall comparison between males and females, no significant difference was noted in DNA damage parameters: Comet TM and MNBC%.

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Purpose: 2-[ 18 F] fluoro-2-deoxy-d-glucose is a positron emitting isotope, which emits 511 keV γ-rays through annihilation process. These γ-rays can induce a variety of DNA damages in animal tissues. It is known that during PET-CT procedure most tissues irradiated with 4-9 mGy absorbed dose and 6-10 mSv whole body effective dose. The biological effects including DNA damages with different dose of fluorine 18 ( 18 F) is still the part of observation and recent research. After knowing the 18 F mediated DNA damage and its repair using time dependent radiation dose study in in-vitro cellular model may clear the understanding of radiation absorbed dose and their side effects including genotoxic effects at specific point of time. Methods: to check the early and late apoptosis in irradiated peripheral blood mononuclear cells (PBMCs), annexin V FITC tagged microscopic imaging was examined. To detect DNA double-strand breaks (DSBs), apoptosis and DNA repair, comet assay and γ-H2AX assay was used. BrdU incorporation assay was also performed to label the fragmented DNA. Results: significant amount of apoptotic cells were observed in PBMC after being irradiated for 120 min with absorbed dose of 8.22 mGy. The appearance of comets and number of foci are increasing in the cells irradiated with 8.22 mGy for 120 min and the amount of FITC tagged BrdU stain percentage confirms the presence of DSBs and apoptosis for longer exposure time (120 min). In DNA repair study, 24 h is the necessary time to repair the damaged cells. Conclusions: our time-and dosedependent study shows that radiation induced DSBs generation and cell apoptosis at low dose radiation of 18 F. 18 F has the capacity to damage DNA and induce apoptosis only if the cells are exposed for the longer period of time. However, all the damages are repaired within 24 h.

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Litsea cubeba is devoured by the ethnic individuals of Arunachal Pradesh in India as food and has been traditionally used for curing different ailments. The purpose of present study was to investigate the antioxidant activities of fruits of L. cubeba using different solvent extracts, quantification of phenolics, toxicity studies and DNA damage protective activities. The antioxidant activities of fruits using five different solvent extracts completed utilizing different in vitro examines. The quantitation of phenolic and polyphenolic compounds in the methanol extract of the fruits was carried out by HPLC. The in vitro haemolytic examination of plant concentrates were completed on rat erythrocytes. Appraisal of cytotoxicity of eatable fruits was assessed by MTT measure. The genotoxicity of the contemplated plant was tried by the single-cell gel electrophoresis comet measure. The DNA defensive impacts of the aqueous extracts of fruits on rodent lymphocyte DNA lesions were likewise assessed with the comet test. The extract obtained by methanol exhibited the highest antioxidant activity. The HPLC examination of the methanol concentrate of the plant demonstrated the occurrence of different phenolic acids and flavonoids like caffeic acid (145.96μg/100mg DE), syringic acid (125.85 μg/100mg DE), ferulic acid (155.89 μg/ 100mg DE), apigenin (28.43 μg/100mg DE), kaempferol (53.41 μg/100mg DE) etc. in various amounts. The consequences of haemolytic lethality, cytotoxicity and genotoxicity of fluid concentrates of the edible plant ensure the security at cell and genomic level. The fluid concentrate of the plant fundamentally repressed DNA harm and these information recommend that the watery concentrate of L. cubeba can forestall oxidative DNA harm to rodent lymphocytes, which is likely because of antioxidant constituents in the concentrate. These outcomes demonstrate that L. cubeba can be utilized in dietary applications with a possibility to diminish oxidative pressure.

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Our previous gene expression studies in a PCB-exposed cohort of young children in Slovakia revealed that early-life exposures to PCBs and other organochlorine compounds were associated with significant alterations across several pathogenetic pathways. The present study was undertaken to further explore the high-throughput qRT-PCR-based gene expression effects by using TaqMan low-density array (TLDA) for selected genes in a sample of 55 children from the cohort. We analyzed the transcriptional changes of 11 genes in relation to PCB and organochlorine pesticide exposure levels (including DDT, DDE, HCH, and HCB), and to BMI and ethnicity in this cohort. The results indicated an overall downregulation of expression of these genes. Maximum downregulation (in fold change) was observed in the ENTPD3 gene, and the minimum level of downregulation was in CYP2D6. As per our multinomial regression model study, downregulation of LEPR gene was significantly directly correlated with all the exposure variables. Downregulation of APC, ARNT, CYP2D6, LEPR, LRP12, and MYC genes was directly correlated with BMI (kg/m2) of the individuals. Gender-specific differences in gene expression were observed in CYP2D6 (p-value 0.0001) and LEPR (p-value 0.028), while downregulation of CYP2D6 (p-value 0.01), LEPR (p-value 0.02), LRP12 (p-value 0.04), and MYC (p-value 0.02) genes was consistently observed in Roma children compared to Caucasians. The investigation of such health disparities must be emphasized in future research, together with interventions to reduce the health consequences of PCB exposures. In this context, we emphasize the importance of biomarker-based approaches to future research on genetic susceptibility to the effects of these compounds.