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119 records – page 1 of 12.

32P-post-labelling of 7-(3-chloro-2-hydroxypropyl)guanine in white blood cells of workers occupationally exposed to epichlorohydrin.

https://arctichealth.org/en/permalink/ahliterature67496
Source
Carcinogenesis. 2000 Feb;21(2):275-80
Publication Type
Article
Date
Feb-2000
Author
K. Plna
S. Osterman-Golkar
E. Nogradi
D. Segerbäck
Author Affiliation
Center for Nutrition and Toxicology, Department of Biosciences, Karolinska Institute, Novum, S-141 57 Huddinge and Department of Molecular Genome Research, Stockholm University, S-106 91 Stockholm, Sweden. kamila.plna2cnt.ki.se
Source
Carcinogenesis. 2000 Feb;21(2):275-80
Date
Feb-2000
Language
English
Publication Type
Article
Keywords
Adult
Alkylating Agents - adverse effects - pharmacology
Biological Markers
Chemical Industry
Chromatography, High Pressure Liquid
Chromatography, Ion Exchange
Comparative Study
DNA Adducts - analysis
DNA Damage
Epichlorohydrin - adverse effects - pharmacology
Guanine - analogs & derivatives - blood
Humans
Isotope Labeling
Leukocytes - chemistry - drug effects
Middle Aged
Occupational Exposure
Occupations
Phosphorus Radioisotopes
Research Support, Non-U.S. Gov't
Sensitivity and specificity
Smoking - epidemiology
Solvents - adverse effects - pharmacology
Sweden
Abstract
Epichlorohydrin (ECH) is a simple 3-carbon epoxide of industrial importance. It has been shown to be genotoxic in several systems and carcinogenic in experimental animals. The aim of the present investigation was to study DNA adducts of ECH as a biomarker of occupational exposure to this chemical. 7-(3-Chloro-2-hydroxypropyl)guanine (7-CHP-guanine) was analysed in DNA from white blood cells using an anion exchange-based adduct enrichment protocol of the (32)P-post-labelling/HPLC-based assay. Blood samples were collected from seven workers handling ECH (exposed), nine workers not handling ECH but normally present in the premises where this chemical is used (potentially exposed) and 13 office and factory workers from locations in the plant where ECH is not handled (controls). 7-CHP-guanine was detected in five of the seven workers exposed to ECH (1.6-7.1 mol/10(9) mol nucleotides) and in two of the nine workers potentially exposed to ECH (0.8-1.5 mol/10(9) mol nucleotides). This adduct was not detected in any of the 13 controls. The difference in adduct levels between exposed workers and controls was statistically significant (Mann-Whitney test, P
PubMed ID
10657968 View in PubMed
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Alpha-particle carcinogenesis in Thorotrast patients: epidemiology, dosimetry, pathology, and molecular analysis.

https://arctichealth.org/en/permalink/ahliterature19345
Source
J Environ Pathol Toxicol Oncol. 2001;20(4):311-5
Publication Type
Article
Date
2001
Author
Y. Ishikawa
I. Wada
M. Fukumoto
Author Affiliation
Department of Pathology, The Cancer Institute, Japanese Foundation for Cancer Research, Tokyo.
Source
J Environ Pathol Toxicol Oncol. 2001;20(4):311-5
Date
2001
Language
English
Publication Type
Article
Keywords
Adult
Aged
Alpha Particles - adverse effects
Carcinogens - adverse effects - pharmacokinetics
Carcinoma, Hepatocellular - epidemiology - etiology
Cause of Death
Cholangiocarcinoma - epidemiology - etiology
DNA Damage
DNA Mutational Analysis
Epidemiologic Studies
Europe - epidemiology
Female
Genes, p53
Half-Life
Hemangiosarcoma - epidemiology - etiology
Humans
Japan - epidemiology
Leukemia - epidemiology - etiology
Liver Cirrhosis - epidemiology - etiology
Liver Neoplasms - epidemiology - etiology
Loss of Heterozygosity
Male
Middle Aged
Radiation Injuries
Research Support, Non-U.S. Gov't
Risk assessment
Thorium Dioxide - adverse effects - pharmacokinetics
United States
Abstract
We studied the alpha-radiation risks in patients who received injections of Thorotrast, an X-ray contrast medium used in Europe, Japan, and the United States from 1930 to 1955. Thorotrast was composed of thorium dioxide (ThO2) and Th-232, a naturally occurring radionuclide. Because the physical half-life of ThO2 is 14 billion years and Thorotrast is hardly eliminated from the body, tissues in which it was deposited are irradiated by alpha-radiation for the entire lifetime of the subject. The dosimetry of Thorotrast patients is very complicated, but currently its reliability is quite high compared with other irradiated populations. The major causes of the death of Thorotrast patients are liver cancer, liver cirrhosis, leukemia, and other cancers. Three histologies of liver cancer are found: cholangiocarcinoma, hepatocellular carcinoma, and angiosarcoma. Although cholangiocarcinoma is the most frequent, angiosarcoma is characteristic of alpha-radiation. Among blood neoplasms with a higher incidence of increase than the general population, erythroleukemia and myelodysplastic syndrome were remarkable. Thorotrast patients exhaled a high concentration of radon (Rn-220), a progeny of Th-232, but no excesses of lung cancer in the patients of Japan, Germany, and Denmark were reported. Mutation analyses of p53 genes and loss of heterozygosity (LOH) studies at 17p locus were performed to characterize the genetic changes in Thorotrast-induced liver tumors. Interestingly, LOH, supposedly corresponding to large deletions was not frequent; most mutations were transitions, also seen in tumors of the general population, suggesting that genetic changes of Thorotrast-induced cancers are mainly delayed mutations, and not the result of the direct effects of radiation.
PubMed ID
11797840 View in PubMed
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Antitumorigenic and cytotoxic properties of an ethanol extract derived from Rhus verniciflua Stokes (RVS).

https://arctichealth.org/en/permalink/ahliterature192645
Source
J Toxicol Environ Health A. 2001 Oct 26;64(4):357-71
Publication Type
Article
Date
Oct-26-2001
Author
D D Kitts
K T Lim
Author Affiliation
Food, Nutrition, and Health, Faculty of Agricultural Sciences, University of British Columbia, Vancouver, Canada. ddkitts@unixg.ubc.ca
Source
J Toxicol Environ Health A. 2001 Oct 26;64(4):357-71
Date
Oct-26-2001
Language
English
Publication Type
Article
Keywords
Animals
Antioxidants - pharmacology
Cell Culture Techniques
Cell Death
Cell Division - drug effects
Chemoprevention
Copper - chemistry
DNA Damage - drug effects
Electrophoresis, Polyacrylamide Gel
Ethanol - chemistry
Free Radicals
Glycoproteins - isolation & purification - pharmacology
HeLa Cells - drug effects
Humans
Hydrogen Peroxide - pharmacology
Iron - pharmacology
Mice
Neoplasms - prevention & control
Neurons - drug effects
Oxidation-Reduction
Plant Extracts - pharmacology
Plasmids
Rhus
Abstract
In this study, the antioxidant, cytotoxic, and antitumorigenic activities of a fractionated, ethanol extract derived from Rhus verniciflua Stokes (RVS), a plant indigenous to Korea, China, and Japan, were determined. Physicochemical analysis and sodium dodecyl sulfate polyacrylamide gel electrophoresis (SDS-PAGE) results indicated that the active component of a Sephadex G-150-fractionated RVS extract (PII fraction) was a copper-containing glycoprotein, possibly a plant laccase. Antioxidant activity of the fractionated RVS extract, observed in both aqueous and lipid in vitro oxidation reactions using 1,1-diphenyl 2-picrylhydrazyl (DPPH) radical, site-specific Fenton-reaction deoxyribose, and a model lipid emulsion test system, indicated an affinity for protection against hydroxyl and peroxyl radicals. Cultured mouse brain neurons were protected against glucose oxidase-induced hydroxyl radical in the presence of the fractionated RVS extract (e.g., 58% protection at 4.9 microM and 95% protection with 22.7 microM RVS). RVS was further shown to protect against in vitro Fenton-reaction-induced single- and double-strand scission in supercoiled plasmid DNA. Further testing for bioactivity of the fractionated RVS extract was based on the affinity to inhibit cell proliferation in cultured HeLa and CT-26 tumor cells. The presence of RVS resulted in 70% cell death after 24 h of incubation in both cell lines at a minimum concentration of 2.48 microM RVS. Data demonstrate multiple bioactive chemopreventative properties of a Sephadex G-150-fractionated extract derived from RVS.
PubMed ID
11693493 View in PubMed
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The application of bioassays in risk assessment of environmental pollution.

https://arctichealth.org/en/permalink/ahliterature223202
Source
Risk Anal. 1992 Sep;12(3):361-5
Publication Type
Article
Date
Sep-1992
Author
T B Lyne
J W Bickham
T. Lamb
J W Gibbons
Author Affiliation
Department of Soil and Crop Sciences, Texas A&M University, College Station 77843.
Source
Risk Anal. 1992 Sep;12(3):361-5
Date
Sep-1992
Language
English
Publication Type
Article
Keywords
Animals
Biological Assay - methods - statistics & numerical data
Biological Markers
DNA Damage
Environmental Monitoring - methods - statistics & numerical data
Environmental Pollution - statistics & numerical data
Humans
Risk
Abstract
Increased contamination of the environment by toxic chemicals has resulted in the need for sensitive assays to be used in risk assessment of polluted sites. Traditional tests are useful to detect and measure concentrations of chemicals in the environment and in tissues. However, physicochemical assays possess deficiencies that impair their use in evaluating complex environmental contamination. We have developed cytogenetic procedures, including chromosomal, micronucleus, and flow cytometric assays, to assess the mutagenic damage of petrochemicals and low-level radioactivity on indigenous terrestrial and aquatic wildlife populations. These procedures are sensitive to the perturbation of DNA that results from exposure to mutagenic contaminants in both field and laboratory studies. The use of natural populations of animals in biomonitoring, combined with traditional chemical assays, will ultimately provide sufficient information to estimate the risk to human health and environmental quality from anthropogenic pollution.
PubMed ID
1410708 View in PubMed
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Assessing the genotoxicity of chronic environmental irradiation by using mitochondrial DNA heteroplasmy in the bank vole (Clethrionomys glareolus) at Chornobyl, Ukraine.

https://arctichealth.org/en/permalink/ahliterature63660
Source
Environ Toxicol Chem. 2002 Jun;21(6):1249-54
Publication Type
Article
Date
Jun-2002
Author
Jeffrey K Wickliffe
Ronald K Chesser
Brenda E Rodgers
Robert J Baker
Author Affiliation
Department of Biological Sciences, Texas Tech University, Lubbock 79409-3131, USA. jeff.wickliffe@ttu.edu
Source
Environ Toxicol Chem. 2002 Jun;21(6):1249-54
Date
Jun-2002
Language
English
Publication Type
Article
Keywords
Accidents, Radiation
Animals
Arvicolinae - genetics - physiology
Biological Markers - analysis
DNA Damage
DNA Mutational Analysis
DNA, Mitochondrial - genetics
Environmental Exposure
Female
Maternal Exposure
Power Plants
Pregnancy
Radioactive Pollutants - adverse effects
Research Support, Non-U.S. Gov't
Research Support, U.S. Gov't, Non-P.H.S.
Risk assessment
Ukraine
Abstract
This study was designed to investigate whether or not chronic exposure to Chornobyl radiation poses a molecular genetic risk to mammals by examining a relatively rapidly evolving genetic system, mitochondrial DNA (mtDNA). More mtDNA mutations (approximately 19%) and an increase in mtDNA heteroplasmy (approximately 5%) occurred in the cytochrome b gene of an exposed mother-embryo set when compared to a relatively unexposed mother-embryo set. However, this increase was not statistically significant (p > 0.05). Our results, in conjunction with previous molecular genetic research on small mammals from Chornobyl, suggest that chronic exposure to environmental ionizing radiation does not increase the number of nucleotide substitutions, as predicted by studies using acute or subacute exposures. Thus, cumulative models of radiation risk would not appear to follow simple linear functions derived from high doses and dose rates. The equivocal nature of research regarding the effects of the Chornobyl accident indicates that future research is warranted such that models of chronic environmental exposure can be developed or refined. Although additional study is required to properly validate mtDNA heteroplasmy as a useful effect biomarker, examination of these data does not indicate that a significant risk to mtDNA exists in native rodents chronically exposed to both internal and external radiation.
PubMed ID
12069310 View in PubMed
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Assessing the level of chromosome aberrations in peripheral blood lymphocytes in long-term resident children under conditions of high exposure to radon and its decay products.

https://arctichealth.org/en/permalink/ahliterature274296
Source
Mutagenesis. 2015 Sep;30(5):677-83
Publication Type
Article
Date
Sep-2015
Author
Vladimir G Druzhinin
Maxim Yu Sinitsky
Aleksey V Larionov
Valentin P Volobaev
Varvara I Minina
Tatiana A Golovina
Source
Mutagenesis. 2015 Sep;30(5):677-83
Date
Sep-2015
Language
English
Publication Type
Article
Keywords
Adolescent
Child
Chromosome Aberrations - radiation effects
DNA - radiation effects
DNA Damage
Female
Humans
Lymphocytes - radiation effects
Male
Radiation Exposure
Radioactivity
Radon - toxicity
Russia
Young Adult
Abstract
In this study, the frequency and spectrum of chromosomal aberrations were analysed in samples of peripheral blood from 372 (mean age = 12.24 ± 2.60 years old) long-term resident children in a boarding school (Tashtagol city, Kemerovo Region, Russian Federation) under conditions of high exposure to radon and its decay products. As a control group, we used blood samples from people living in Zarubino village (Kemerovo Region, Russian Federation). We discovered that the average frequencies of single and double fragments, chromosomal exchanges, total number of aberrations, chromatid type, chromosome type and all types of aberrations were significantly increased in the exposed group. This is evidence of considerable genotoxicity to children living under conditions of high exposure to radon compared to children living under ecological conditions without increased radon radiation.
PubMed ID
25904585 View in PubMed
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Assessment of DNA damage in underground coal miners using the cytokinesis-block micronucleus assay in peripheral blood lymphocytes.

https://arctichealth.org/en/permalink/ahliterature285259
Source
Mutagenesis. 2016 Nov;31(6):669-675
Publication Type
Article
Date
Nov-2016
Author
Maxim Yu Sinitsky
Varvara I Minina
Nikolay I Gafarov
Maxim A Asanov
Aleksey V Larionov
Anastasia V Ponasenko
Valentin P Volobaev
Vladimir G Druzhinin
Source
Mutagenesis. 2016 Nov;31(6):669-675
Date
Nov-2016
Language
English
Publication Type
Article
Keywords
Adult
Coal - toxicity
DNA Damage
Dust
Humans
Lymphocytes - pathology
Male
Micronuclei, Chromosome-Defective - chemically induced
Micronucleus Tests
Middle Aged
Miners
Occupational Exposure
Russia
Abstract
Coal miners are exposed to coal dust, containing mineral particles, inorganic compounds and polycyclic aromatic hydrocarbons, and to ionizing radiation. These factors can induce oxidative stress and promote inflammation that leads to DNA damage. The aim of this investigation is to analyse the degree of DNA damage in miners working in underground coal mines in Kemerovo Region (Russian Federation) using the cytokinesis-block micronucleus assay (CBMN) in peripheral blood lymphocytes. The exposed group included 143 coal miners (mean age = 50.11±7.36 years; mean length of service in coal mining conditions = 23.26±9.66 years). As a control group, we have used venous blood extracted from 127 healthy non-exposed men. The mean age in this group was 47.67±8.45 years. We have discovered that coal miners are characterized by a significant increase in the frequency of binucleated lymphocytes with micronuclei (MN), nucleoplasmic bridges (NPBs) and protrusions (NBUDs) compared to non-exposed donors. In addition, we report, for the first time, a reduction of cell proliferation in a cohort of coal miners. These data are evidence of the genotoxic and cytostatic effects of occupational harmful factors of the coal mining industry. No correlation between the level of chromosome damage and age, smoking status or length of service in coal mining conditions were discovered. We suggest that the CBMN assay would be useful in biomonitoring studies to monitor hygiene and prevention strategies in occupational settings in coal mining countries.
PubMed ID
27530330 View in PubMed
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Assessment of in vitro cyto/genotoxicity of sequentially treated electroplating effluent on the human hepatocarcinoma HuH-7 cell line.

https://arctichealth.org/en/permalink/ahliterature104977
Source
Mutat Res Genet Toxicol Environ Mutagen. 2014 Mar 1;762:9-16
Publication Type
Article
Date
Mar-1-2014
Author
Umesh Chandra Naik
Mihir Tanay Das
Swati Sauran
Indu Shekhar Thakur
Author Affiliation
School of Environmental Sciences, Jawaharlal Nehru University, New Delhi 110 067, India. Electronic address: umeshbiology@gmail.com.
Source
Mutat Res Genet Toxicol Environ Mutagen. 2014 Mar 1;762:9-16
Date
Mar-1-2014
Language
English
Publication Type
Article
Keywords
Biodegradation, Environmental
Cell Line, Tumor
Cell Survival - drug effects
Charcoal - chemistry
Comet Assay
DNA Damage
Electroplating
Environmental Pollutants - chemistry - toxicity
Humans
Industrial Waste - adverse effects - analysis
Metals, Heavy - chemistry - toxicity
Mutagens - chemistry - toxicity
Water Purification - methods
Abstract
The present study compares in vitro toxicity of electroplating effluent after the batch treatment process with that obtained after the sequential treatment process. Activated charcoal prepared from sugarcane bagasse through chemical carbonization, and tolerant indigenous bacteria, Bacillus sp. strain IST105, were used individually and sequentially for the treatment of electroplating effluent. The sequential treatment involving activated charcoal followed by bacterial treatment removed 99% of Cr(VI) compared with the batch processes, which removed 40% (charcoal) and 75% (bacteria), respectively. Post-treatment in vitro cyto/genotoxicity was evaluated by the MTT test and the comet assay in human HuH-7 hepatocarcinoma cells. The sequentially treated sample showed an increase in LC50 value with a 6-fold decrease in comet-assay DNA migration compared with that of untreated samples. A significant decrease in DNA migration and an increase in LC50 value of treated effluent proved the higher effectiveness of the sequential treatment process over the individual batch processes.
PubMed ID
24525376 View in PubMed
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Association between 8-oxo-7,8-dihydro-2'-deoxyguanosine excretion and risk of postmenopausal breast cancer: nested case-control study.

https://arctichealth.org/en/permalink/ahliterature114047
Source
Cancer Epidemiol Biomarkers Prev. 2013 Jul;22(7):1289-96
Publication Type
Article
Date
Jul-2013
Author
Steffen Loft
Anja Olsen
Peter Møller
Henrik E Poulsen
Anne Tjønneland
Author Affiliation
Department of Public Health, Section of Enviromental Health, Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark. stl@sund.ku.dk
Source
Cancer Epidemiol Biomarkers Prev. 2013 Jul;22(7):1289-96
Date
Jul-2013
Language
English
Publication Type
Article
Keywords
Breast Neoplasms - epidemiology - genetics - metabolism - urine
Case-Control Studies
Cohort Studies
DNA Damage
Denmark - epidemiology
Deoxyguanosine - analogs & derivatives - urine
Diet
Female
Follow-Up Studies
Humans
Middle Aged
Oxidative Stress - genetics - physiology
Postmenopause - genetics - urine
Prospective Studies
Receptors, Estrogen - biosynthesis
Risk factors
Tumor Markers, Biological - urine
Abstract
Oxidative stress may be important in carcinogenesis and a possible risk factor for breast cancer. The urinary excretion of oxidatively generated biomolecules, such as 8-oxo-7,8-dihydro-2'-deoxyguanosine (8-oxodG), represents biomarkers of oxidative stress, reflecting the rate of global damage to DNA in steady state.
In a nested case-control design, we examined associations between urinary excretion of 8-oxodG and risk of breast cancer in a population-based cohort of 24,697 postmenopausal women aged 50 to 64 years with 3 to 7 years follow-up. The accruing cases of breast cancer were matched to controls by age at diagnosis, baseline age, and hormone replacement therapy (HRT). Spot urine samples collected at entry was analyzed for 8-oxodG by high-performance liquid chromatography with electrochemical detection. Incidence rate ratio (IRR; 95% confidence intervals) based on 336 matched pairs with all information was estimated per unit increase in 8-oxodG divided by creatinine for all and estrogen receptor (ER) positive and negative breast cancers.
There was a borderline significant positive association between 8-oxodG and risk of all breast cancer (IRR: 1.08; 1.00-1.17 per unit increase in nmol/mmol creatinine). This association was significant with respect to the risk of ER-positive cancer (IRR: 1.11; 1.01-1.23) and among women not using HRT (IRR: 1.11; 0.97-1.26) or with low dietary iron intake (IRR: 1.10; 1.06-1.37 per unit increase) for all breast cancer.
We observed positive association between 8-oxodG excretion and risk of especially ER-positive breast cancer.
Our results suggest that oxidative stress with damage to DNA is important for the development of breast cancer.
PubMed ID
23658396 View in PubMed
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Biological low-dose radiation effects.

https://arctichealth.org/en/permalink/ahliterature24757
Source
Mutat Res. 1991 Sep;258(2):191-205
Publication Type
Article
Date
Sep-1991
Author
P. Oftedal
Author Affiliation
Division of General Genetics, University of Oslo, Norway.
Source
Mutat Res. 1991 Sep;258(2):191-205
Date
Sep-1991
Language
English
Publication Type
Article
Keywords
Animals
Bone Marrow - radiation effects
Child
Child Development - radiation effects
DNA Damage
DNA Repair
Dose-Response Relationship, Radiation
Humans
Models, Biological
Neoplasms, Radiation-Induced - epidemiology
Norway - epidemiology
Radiation Protection - standards
Rats
Thyroid Neoplasms - epidemiology
Abstract
It is theorized that biological responses to ionizing radiation in the low dose range are determined according to a doubly dichotomous pattern. Energy depositions fall into 2 categories: events at thermal energy levels where they may be experienced by cells as rates even at background exposure conditions, and events at energy levels of the order of 10-100 eV where damage to DNA may be caused. Variations in background exposure intensity may or may not lead preemptively to changes in the cell's capacity for response to radiation damage. High-level energy depositions lead post hoc to an initial stabilizing reaction largely leading to the fixation of the initial DNA damage, and to a subsequent restorative or palliative repair process. This model entails reinterpretation of some experimental results. The model has implications for the relationship between scientific analysis of low-dose effects and the regulatory needs for simplicity and homogeneity in risk evaluation. This represents a new challenge for the acceptability of radiation protection norms.
Notes
Comment In: Mutat Res. 1992 Dec;298(2):141-31282211
PubMed ID
1715511 View in PubMed
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119 records – page 1 of 12.