scholarly journals Recent Physical Activity in Relation to DNA Damage and Repair Using the Comet Assay

2014 ◽  
Vol 11 (4) ◽  
pp. 770-776 ◽  
Author(s):  
Stephanie Whisnant Cash ◽  
Shirley A.A. Beresford ◽  
Thomas L. Vaughan ◽  
Patrick J. Heagerty ◽  
Leslie Bernstein ◽  
...  
Keyword(s):  
Physical Activity ◽  
Dna Damage ◽  
Dna Repair ◽  
Comet Assay ◽  
High Intensity ◽  
Total Activity ◽  
Washington State ◽  
Dna Damage And Repair ◽  
Activity Intensity ◽  
Very High

Background:Limited evidence suggests that very high-intensity exercise is positively associated with DNA damage but moderate exercise may be associated with DNA repair.Methods:Participants were 220 healthy, Washington State 50- to 76-year-olds in the validity/biomarker substudy of the VITamins And Lifestyle (VITAL) cohort, who provided blood samples and completed questionnaires assessing recent physical activity and demographic and health factors. Measures included nested activity subsets: total activity, moderate- plus high-intensity activity, and high-intensity activity. DNA damage (n = 122) and repair (n = 99) were measured using the comet assay. Multivariate linear regression was used to estimate regression coefficients and associated 95% confidence intervals (CIs) for relationships between MET-hours per week of activity and each DNA outcome (damage, and 15- and 60-minute repair capacities).Results:DNA damage was not associated with any measure of activity. However, 60-minute DNA repair was positively associated with both total activity (β = 0.21, 95% CI: 0.0057–0.412; P = .044) and high-intensity activity (β = 0.31, 95% CI: 0.20–0.60; P = .036), adjusting for age, sex, BMI, and current multivitamin use.Conclusions:This study is the first to assess broad ranges of activity intensity levels related to DNA damage and repair. Physical activity was unrelated to DNA damage but was associated with increased repair.

Expression of critical genes used as prognostic biomarkers and DNA damage in lymphocytes from breast cancer patients

2006 ◽  
Vol 24 (18_suppl) ◽  
pp. 10641-10641 ◽  
Author(s):  
F. Franke ◽  
M. Agnoletto ◽  
J. Saffi ◽  
T. Guecheva
Keyword(s):  
Breast Cancer ◽  
Dna Damage ◽  
Dna Repair ◽  
Comet Assay ◽  
Cancer Patients ◽  
Peripheral Blood ◽  
Peripheral Blood Lymphocytes ◽  
Breast Cancer Patients ◽  
Dna Damage And Repair ◽  
Blood Lymphocytes

10641 Breast cancer is the most common malignancy among women and its rate of mortality is still high. The increase knowledge of breast cancer biology is heaving great impact on determining the clinical prognosis and response to treatment. Impaired DNA repair may elevate the risk of malignant transformation of breast cells due to the accumulation of spontaneous mutations in target genes and increasing susceptibility to exogenous carcinogens. The present study was designed to evaluate the relationship between DNA damage and expression of some critical genes including TP53, c-ERBB2, ER (Estrogen Receptor) and PR (Progesterone Receptor) in breast cancer. Blood samples were obtained from female patients with diagnosed breast cancer before chemotherapy as well as from healthy individuals, and were processed in 24 hours. To evaluate the role of DNA repair in breast cancer we determined the level of DNA damage and the capacity to remove DNA damage induced by hydrogen peroxide in the peripheral blood lymphocytes. For this purpose the alkaline version of the comet assay, which provides a sensitive tool to investigate DNA damage and repair, was applied. The level of basal DNA damage was higher in breast cancer patients compared to the control group. Considerable inter-individual variations of DNA damage and repair in breast cancer patients were observed both before and after the treatment. The correlation between DNA damage in peripheral blood and expression of p53, c-erbB-2, PR and ER was analyzed. This preliminary study indicates that the DNA damage accumulation, observed in peripheral blood lymphocytes of breast cancer patients in early stages, could be attributed to impaired DNA repair. Our results suggest that DNA damage, as evaluated by the comet assay, seems to be useful molecular biomarker for monitoring ongoing exposures to DNA damaging agents. Such a research on the mutagen sensitivity and efficacy of DNA repair could impact on the development of new diagnostic and screening strategies. Work Supported by FAPERGS and GENOTOX (UFRGS). No significant financial relationships to disclose.

DNA damage and repair capacity by comet assay in lymphocytes of white-collar active smokers and passive smokers (non- and ex-smokers) at workplace

2006 ◽  
Vol 167 (2) ◽  
pp. 131-141 ◽  
Author(s):  
Maria Enrica Fracasso ◽  
Denise Doria ◽  
Paola Franceschetti ◽  
Luigi Perbellini ◽  
Luciano Romeo
Keyword(s):  
Dna Damage ◽  
Comet Assay ◽  
White Collar ◽  
Repair Capacity ◽  
Dna Damage And Repair

scholarly journals Impacts of vigorous and non-vigorous activity on daily energy expenditure

2003 ◽  
Vol 62 (3) ◽  
pp. 645-650 ◽  
Author(s):  
Klaas R. Westerterp
Keyword(s):  
Physical Activity ◽  
Body Size ◽  
Energy Expenditure ◽  
Exercise Training ◽  
Physical Activity Level ◽  
High Intensity ◽  
Activity Level ◽  
Daily Energy Expenditure ◽  
Activity Intensity ◽  
Daily Energy

Activity intensity is a potential determinant of activity-induced energy expenditure. Tri-axial accelerometery is the most objective measurement technique for the assessment of activity intensity, in combination with doubly-labelled water for the measurement of energy expenditure under free-living conditions. Data on the effects of subject characteristics, including body size and age, and exercise training on the relationship between activity intensity and daily energy expenditure are reviewed. Average daily metabolic rate and non-basal energy expenditure are positively related to body size. The duration and intensity of physical activities do not need to be equivalent to the energy spent on activity. Obese subjects spend more energy on physical activity but can perform fewer activities, especially high-intensity (weight-bearing) activities, because of their higher body weight. Physical activity generally declines gradually from about 60 years of age onwards. Most subjects >80 years have an activity level well below the level defined for sedentary middle-aged adults. Spending relatively more time on low-intensity activities has a negative effect on the mean physical activity level. To obtain a higher physical activity level does not necessarily imply high-intensity activities. In an average subject 25% of the activity-induced energy expenditure may be attributed to high-intensity activities. Exercise training, as a form of high-intensity activity, affects the physical activity level more in younger subjects than in elderly subjects.

Variability in DNA repair and individual susceptibility to genotoxins

1995 ◽  
Vol 41 (12) ◽  
pp. 1848-1853 ◽  
Author(s):  
S A Kyrtopoulos
Keyword(s):  
Dna Damage ◽  
Dna Repair ◽  
Protective Role ◽  
Interindividual Variation ◽  
Human Populations ◽  
Cytostatic Drugs ◽  
Dna Damage And Repair ◽  
Cellular Protection ◽  
Methylated Dna ◽  
Methylating Agents

Abstract DNA repair is an important mechanism of cellular protection from the effects of genotoxic chemicals. Although extensive evidence from studies in experimental systems indicates that variation in DNA repair can significantly influence susceptibility to genotoxins, corresponding studies in human populations are so far limited, mainly because of methodological difficulties. One system, using observations of the accumulation and repair of DNA damage in cancer patients treated with alkylating cytostatic drugs, has provided useful information for assessing the effects of interindividual variation in DNA repair activity on the induction of genotoxic effects in humans. The most detailed studies of this kind have been carried out on patients with cancer (i.e., Hodgkin disease, malignant melanoma) treated with the methylating cytostatic drugs procarbazine or dacarbazine; these studies have provided detailed information on dose-response relationships. They have also demonstrated the protective role of the repair enzyme O6-alkylguanine-DNA alkyltransferase against the accumulation of the premutagenic methylated DNA lesion O6-methylguanine in patients' DNA. Given the strong evidence that exposure of the general population to environmental methylating agents may be extensive, as indicated by the frequent discovery of methylated DNA adducts in human DNA, data on DNA damage and repair in alkylating drug-treated patients and their modulation by host factors may prove useful in efforts to assess the possible carcinogenic risks posed by exposure to environmental methylating agents.

scholarly journals Mutational signatures are jointly shaped by DNA damage and repair

2020 ◽  
Vol 11 (1) ◽  
Author(s):  
Nadezda V. Volkova ◽  
Bettina Meier ◽  
Víctor González-Huici ◽  
Simone Bertolini ◽  
Santiago Gonzalez ◽  
...  
Keyword(s):  
Dna Damage ◽  
Dna Repair ◽  
Excision Repair ◽  
Point Mutations ◽  
Mutational Signatures ◽  
Dna Damage And Repair ◽  
C Elegans ◽  
Dna Repair Deficiency ◽  
Dna Alterations ◽  
Repair Pathways

AbstractCells possess an armamentarium of DNA repair pathways to counter DNA damage and prevent mutation. Here we use C. elegans whole genome sequencing to systematically quantify the contributions of these factors to mutational signatures. We analyse 2,717 genomes from wild-type and 53 DNA repair defective backgrounds, exposed to 11 genotoxins, including UV-B and ionizing radiation, alkylating compounds, aristolochic acid, aflatoxin B1, and cisplatin. Combined genotoxic exposure and DNA repair deficiency alters mutation rates or signatures in 41% of experiments, revealing how different DNA alterations induced by the same genotoxin are mended by separate repair pathways. Error-prone translesion synthesis causes the majority of genotoxin-induced base substitutions, but averts larger deletions. Nucleotide excision repair prevents up to 99% of point mutations, almost uniformly across the mutation spectrum. Our data show that mutational signatures are joint products of DNA damage and repair and suggest that multiple factors underlie signatures observed in cancer genomes.

scholarly journals DNA Repair Biosensor-Identified DNA Damage Activities of Endophyte Extracts from Garcinia cowa

Biomolecules ◽  
2020 ◽  
Vol 10 (12) ◽  
pp. 1680
Author(s):  
Tassanee Lerksuthirat ◽  
Rakkreat Wikiniyadhanee ◽  
Sermsiri Chitphuk ◽  
Wasana Stitchantrakul ◽  
Somponnat Sampattavanich ◽  
...  
Keyword(s):  
Dna Damage ◽  
Dna Repair ◽  
Fluorescent Proteins ◽  
Strand Break ◽  
Control Group ◽  
Focus Formation ◽  
Dna Damage And Repair ◽  
Biological Compounds ◽  
Repair Pathways ◽  
Garcinia Cowa

Recent developments in chemotherapy focus on target-specific mechanisms, which occur only in cancer cells and minimize the effects on normal cells. DNA damage and repair pathways are a promising target in the treatment of cancer. In order to identify novel compounds targeting DNA repair pathways, two key proteins, 53BP1 and RAD54L, were tagged with fluorescent proteins as indicators for two major double strand break (DSB) repair pathways: non-homologous end-joining (NHEJ) and homologous recombination (HR). The engineered biosensor cells exhibited the same DNA repair properties as the wild type. The biosensor cells were further used to investigate the DNA repair activities of natural biological compounds. An extract from Phyllosticta sp., the endophyte isolated from the medicinal plant Garcinia cowa Roxb. ex Choisy, was tested. The results showed that the crude extract induced DSB, as demonstrated by the increase in the DNA DSB marker γH2AX. The damaged DNA appeared to be repaired through NHEJ, as the 53BP1 focus formation in the treated fraction was higher than in the control group. In conclusion, DNA repair-based biosensors are useful for the preliminary screening of crude extracts and biological compounds for the identification of potential targeted therapeutic drugs.

Sign in / Sign up

Export Citation Format

Share Document