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Article ; Online: Optimizing the Comet Assay-Based In Vitro DNA Repair Assay for Placental Tissue: A Pilot Study with Pre-Eclamptic Patients.

Mircheva, Anastasiya / Vangrieken, Philippe / Al-Nasiry, Salwan / van Schooten, Frederik-Jan / Godschalk, Roger W L / Langie, Sabine A S

International journal of molecular sciences

2023 Volume 25, Issue 1

Abstract: The comet assay-based in vitro DNA repair assay has become a common tool for quantifying base excision repair (BER) activity in human lymphocytes or cultured cells. Here, we optimized the protocol for studying BER in human placental tissue because the ... ...

Abstract	The comet assay-based in vitro DNA repair assay has become a common tool for quantifying base excision repair (BER) activity in human lymphocytes or cultured cells. Here, we optimized the protocol for studying BER in human placental tissue because the placenta is a non-invasive tissue for biomonitoring of early-life exposures, and it can be used to investigate molecular mechanisms associated with prenatal disorders. The optimal protein concentration of placental protein extracts for optimal damage recognition and incision was 2 mg protein/mL. The addition of aphidicolin did not lead to reduced non-specific incisions and was, therefore, not included in the optimized protocol. The interval between sample collection and analysis did not affect BER activity up to 70 min. Finally, this optimized protocol was tested on pre-eclamptic (PE) placental tissues (
MeSH term(s)	Pregnancy ; Humans ; Female ; Pilot Projects ; Comet Assay ; Prospective Studies ; Placenta ; DNA Repair ; Pre-Eclampsia/genetics
Language	English
Publishing date	2023-12-22
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2019364-6
ISSN	1422-0067 ; 1422-0067 ; 1661-6596
ISSN (online)	1422-0067
ISSN	1422-0067 ; 1661-6596
DOI	10.3390/ijms25010187
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Article: Maternal exposure to genistein during pregnancy and oxidative DNA damage in testes of male mouse offspring.

Godschalk, Roger W L / Janssen, Margit C M / Vanhees, Kimberly / van Doorn-Khosrovani, Sahar Barjesteh van Waalwijk / van Schooten, Frederik-Jan

Frontiers in nutrition

2022 Volume 9, Page(s) 904368

Abstract: Background: Genistein is a dietary supplement with phyto-estrogenic properties. Therefore, high intake of genistein during pregnancy may have adverse effects on the genetic integrity of testes and germ cells of male offspring. In this study, we examined ...

Abstract	Background: Genistein is a dietary supplement with phyto-estrogenic properties. Therefore, high intake of genistein during pregnancy may have adverse effects on the genetic integrity of testes and germ cells of male offspring. In this study, we examined whether maternal exposure to genistein during pregnancy induced oxidative DNA damage in the male germline at adolescence. Methods: Atm Results: Intake of genistein during pregnancy increased oxidative DNA damage in testes of offspring, especially in heterozygous Conclusion: These data indicate that prenatal exposure to genistein altered gene expression and increased DNA damage in testes and sperm of adolescent male offspring. These effects of genistein on DNA damage in later life coincided with alterations in DNA methylation.
Language	English
Publishing date	2022-07-18
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2776676-7
ISSN	2296-861X
ISSN	2296-861X
DOI	10.3389/fnut.2022.904368
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Article: Maternal fatty acid status during pregnancy versus offspring inflammatory markers: a canonical correlation analysis of the MEFAB cohort.

Rouschop, Sven H / Smolinska, Agnieszka / Gielen, Marij / de Groot, Renate H M / Zeegers, Maurice P / Opperhuizen, Antoon / van Schooten, Frederik J / Godschalk, Roger W

Frontiers in nutrition

2023 Volume 10, Page(s) 1264278

Abstract: The development of inflammatory lung disorders in children may be related to maternal fatty acid intake during pregnancy. We therefore examined maternal fatty acid (FA) status during pregnancy and its associations with inflammatory markers and lung ... ...

Abstract	The development of inflammatory lung disorders in children may be related to maternal fatty acid intake during pregnancy. We therefore examined maternal fatty acid (FA) status during pregnancy and its associations with inflammatory markers and lung conditions in the child by analyzing data from the MEFAB cohort using multivariate canonical correlation analysis (CCA). In the MEFAB cohort, 39 different phospholipid FAs were measured in maternal plasma at 16, 22 and 32 weeks of pregnancy, and at day of birth. Child inflammatory markers and self-reported doctor diagnosis of inflammatory lung disorders were assessed at 7 years of age. Using CCA, we found that maternal FA levels during pregnancy were significantly associated with child inflammatory markers at 7 years of age and that Mead acid (20:3n-9) was the most important FA for this correlation. To further verify the importance of Mead acid, we examined the relation between maternal Mead acid levels at the day of birth with the development of inflammatory lung disorders in children at age 7. After stratification for the child's sex, maternal Mead acid levels at day of birth were significantly related with self-reported doctor diagnosis of asthma and lung infections in boys, and bronchitis and total number of lung disorders in girls. Future studies should investigate whether the importance of Mead acid in the relation between maternal FA status and inflammation and lung disorders in the child is due to its role as biomarker for essential fatty acid deficiency or due to its own biological function as pro-inflammatory mediator.
Language	English
Publishing date	2023-10-19
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2776676-7
ISSN	2296-861X
ISSN	2296-861X
DOI	10.3389/fnut.2023.1264278
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Article ; Online: In utero Exposure to Genotoxicants Leading to Genetic Mosaicism: An Overlooked Window of Susceptibility in Genetic Toxicology Testing?

Godschalk, Roger W L / Yauk, Carole L / van Benthem, Jan / Douglas, George R / Marchetti, Francesco

Environmental and molecular mutagenesis

2019 Volume 61, Issue 1, Page(s) 55–65

Abstract: In utero development represents a sensitive window for the induction of mutations. These mutations may subsequently expand clonally to populate entire organs or anatomical structures. Although not all adverse mutations will affect tissue structure or ... ...

Abstract	In utero development represents a sensitive window for the induction of mutations. These mutations may subsequently expand clonally to populate entire organs or anatomical structures. Although not all adverse mutations will affect tissue structure or function, there is growing evidence that clonally expanded genetic mosaics contribute to various monogenic and complex diseases, including cancer. We posit that genetic mosaicism is an underestimated potential health problem that is not fully addressed in the current regulatory genotoxicity testing paradigm. Genotoxicity testing focuses exclusively on adult exposures and thus may not capture the complexity of genetic mosaicisms that contribute to human disease. Numerous studies have shown that conversion of genetic damage into mutations during early developmental exposures can result in much higher mutation burdens than equivalent exposures in adults in certain tissues. Therefore, we assert that analysis of genetic effects caused by in utero exposures should be considered in the current regulatory testing paradigm, which is possible by harmonization with current reproductive/developmental toxicology testing strategies. This is particularly important given the recent proposed paradigm change from simple hazard identification to quantitative mutagenicity assessment. Recent developments in sequencing technologies offer practical tools to detect mutations in any tissue or species. In addition to mutation frequency and spectrum, these technologies offer the opportunity to characterize the extent of genetic mosaicism following exposure to mutagens. Such integration of new methods with existing toxicology guideline studies offers the genetic toxicology community a way to modernize their testing paradigm and to improve risk assessment for vulnerable populations. Environ. Mol. Mutagen. 61:55-65, 2020. © 2019 The Authors. Environmental and Molecular Mutagenesis published by Wiley Periodicals, Inc. on behalf of Environmental Mutagen Society.
MeSH term(s)	Animals ; Female ; Genetic Testing/methods ; Humans ; Male ; Maternal Exposure/adverse effects ; Mosaicism/drug effects ; Mutagenesis/drug effects ; Mutagenicity Tests/methods ; Mutagens/toxicity ; Mutation/drug effects ; Mutation Rate ; Paternal Exposure/adverse effects ; Pregnancy ; Prenatal Exposure Delayed Effects/genetics
Chemical Substances	Mutagens
Language	English
Publishing date	2019-12-05
Publishing country	United States
Document type	Journal Article
ZDB-ID	639145-x
ISSN	1098-2280 ; 0893-6692
ISSN (online)	1098-2280
ISSN	0893-6692
DOI	10.1002/em.22347
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Article: Polymorphisms in the mTOR-PI3K-Akt pathway, energy balance-related exposures and colorectal cancer risk in the Netherlands Cohort Study.

Simons, Colinda C J M / Schouten, Leo J / Godschalk, Roger W L / van Schooten, Frederik-Jan / Stoll, Monika / Van Steen, Kristel / van den Brandt, Piet A / Weijenberg, Matty P

BioData mining

2022 Volume 15, Issue 1, Page(s) 2

Abstract: Background: The mTOR-PI3K-Akt pathway influences cell metabolism and (malignant) cell growth. We generated sex-specific polygenic risk scores capturing natural variation in 7 out of 10 top-ranked genes in this pathway. We studied the scores directly and ...

Abstract	Background: The mTOR-PI3K-Akt pathway influences cell metabolism and (malignant) cell growth. We generated sex-specific polygenic risk scores capturing natural variation in 7 out of 10 top-ranked genes in this pathway. We studied the scores directly and in interaction with energy balance-related factors (body mass index (BMI), trouser/skirt size, height, physical activity, and early life energy restriction) in relation to colorectal cancer (CRC) risk in the Netherlands Cohort Study (NLCS) (n=120,852). The NLCS has a case-cohort design and 20.3 years of follow-up. Participants completed a baseline questionnaire on diet and cancer in 1986 when 55-69 years old. ~75% of the cohort returned toenail clippings used for DNA isolation and genotyping (n subcohort=3,793, n cases=3,464). To generate the scores, the dataset was split in two and risk alleles were defined and weighted based on sex-specific associations with CRC risk in the other dataset half, because there were no SNPs in the top-ranked genes associated with CRC risk in previous genome-wide association studies at a significance level p<110 Results:* Cox regression analyses showed positive associations between the sex-specific polygenic risk scores and colon but not rectal cancer risk in men and women, with hazard ratios for continuously modeled scores close to 1.10. There was no modifying effect observed of the scores on associations between the energy balance-related factors and CRC risk. However, BMI (in men), non-occupational physical activity (in women), and height (in men and women) were associated with the risk of CRC, in particular (proximal and distal) colon cancer, in the direction as expected in the lower tertiles of the sex-specific polygenic risk scores. Conclusions: Current data suggest that the mTOR-PI3K-Akt pathway may be involved in colon cancer development. This study thereby sheds more light on colon cancer etiology through use of genetic variation in the mTOR-PI3K-Akt pathway.
Language	English
Publishing date	2022-01-10
Publishing country	England
Document type	Journal Article
ZDB-ID	2438773-3
ISSN	1756-0381
ISSN	1756-0381
DOI	10.1186/s13040-021-00286-3
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Article ; Online: Perinatal High-Fat Diet Influences Ozone-Induced Responses on Pulmonary Oxidant Status and the Molecular Control of Mitophagy in Female Rat Offspring.

Rouschop, Sven H / Snow, Samantha J / Kodavanti, Urmila P / Drittij, Marie-José / Maas, Lou M / Opperhuizen, Antoon / van Schooten, Frederik J / Remels, Alexander H / Godschalk, Roger W

International journal of molecular sciences

2021 Volume 22, Issue 14

Abstract: Previous research has shown that a perinatal obesogenic, high-fat diet (HFD) is able to exacerbate ozone-induced adverse effects on lung function, injury, and inflammation in offspring, and it has been suggested that mitochondrial dysfunction is ... ...

Abstract	Previous research has shown that a perinatal obesogenic, high-fat diet (HFD) is able to exacerbate ozone-induced adverse effects on lung function, injury, and inflammation in offspring, and it has been suggested that mitochondrial dysfunction is implicated herein. The aim of this study was to investigate whether a perinatal obesogenic HFD affects ozone-induced changes in offspring pulmonary oxidant status and the molecular control of mitochondrial function. For this purpose, female Long-Evans rats were fed a control diet or HFD before and during gestation, and during lactation, after which the offspring were acutely exposed to filtered air or ozone at a young-adult age (forty days). Directly following this exposure, the offspring lungs were examined for markers related to oxidative stress; oxidative phosphorylation; and mitochondrial fusion, fission, biogenesis, and mitophagy. Acute ozone exposure significantly increased pulmonary oxidant status and upregulated the molecular machinery that controls receptor-mediated mitophagy. In female offspring, a perinatal HFD exacerbated these responses, whereas in male offspring, responses were similar for both diet groups. The expression of the genes and proteins involved in oxidative phosphorylation and mitochondrial biogenesis, fusion, and fission was not affected by ozone exposure or perinatal HFD. These findings suggest that a perinatal HFD influences ozone-induced responses on pulmonary oxidant status and the molecular control of mitophagy in female rat offspring.
MeSH term(s)	Animals ; Animals, Newborn ; Diet, High-Fat/adverse effects ; Female ; Gene Expression Profiling ; Lung/metabolism ; Lung/pathology ; Male ; Maternal Nutritional Physiological Phenomena ; Mitochondria/metabolism ; Mitochondria/pathology ; Mitophagy ; Oxidants/metabolism ; Oxidative Phosphorylation ; Oxidative Stress ; Ozone/adverse effects ; Pregnancy ; Prenatal Exposure Delayed Effects/etiology ; Prenatal Exposure Delayed Effects/pathology ; Rats ; Rats, Long-Evans
Chemical Substances	Oxidants ; Ozone (66H7ZZK23N)
Language	English
Publishing date	2021-07-14
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2019364-6
ISSN	1422-0067 ; 1422-0067 ; 1661-6596
ISSN (online)	1422-0067
ISSN	1422-0067 ; 1661-6596
DOI	10.3390/ijms22147551
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Article ; Online: DNA repair as a human biomonitoring tool: Comet assay approaches.

Azqueta, Amaya / Langie, Sabine A S / Boutet-Robinet, Elisa / Duthie, Susan / Ladeira, Carina / Møller, Peter / Collins, Andrew R / Godschalk, Roger W L

Mutation research. Reviews in mutation research

2019 Volume 781, Page(s) 71–87

Abstract: The comet assay offers the opportunity to measure both DNA damage and repair. Various comet assay based methods are available to measure DNA repair activity, but some requirements should be met for their effective use in human biomonitoring studies. ... ...

Abstract	The comet assay offers the opportunity to measure both DNA damage and repair. Various comet assay based methods are available to measure DNA repair activity, but some requirements should be met for their effective use in human biomonitoring studies. These conditions include i) robustness of the assay, ii) sources of inter- and intra-individual variability must be known, iii) DNA repair kinetics should be assessed to optimize sampling timing; and iv) DNA repair in accessible surrogate tissues should reflect repair activity in target tissues prone to carcinogenic effects. DNA repair phenotyping can be performed on frozen and fresh samples, and is a more direct measurement than genomic or transcriptomic approaches. There are mixed reports concerning the regulation of DNA repair by environmental and dietary factors. In general, exposure to genotoxic agents did not change base excision repair (BER) activity, whereas some studies reported that dietary interventions affected BER activity. On the other hand, in vitro and in vivo studies indicated that nucleotide excision repair (NER) can be altered by exposure to genotoxic agents, but studies on other life style related factors, such as diet, are rare. Thus, crucial questions concerning the factors regulating DNA repair and inter-individual variation remain unanswered. Intra-individual variation over a period of days to weeks seems limited, which is favourable for DNA repair phenotyping in biomonitoring studies. Despite this reported low intra-individual variation, timing of sampling remains an issue that needs further investigation. A correlation was reported between the repair activity in easily accessible peripheral blood mononuclear cells (PBMCs) and internal organs for both NER and BER. However, no correlation was found between tumour tissue and blood cells. In conclusion, although comet assay based approaches to measure BER/NER phenotypes are feasible and promising, more work is needed to further optimize their application in human biomonitoring and intervention studies.
MeSH term(s)	Animals ; Biological Monitoring/methods ; Comet Assay/methods ; DNA Damage/drug effects ; DNA Damage/genetics ; DNA Repair/drug effects ; DNA Repair/genetics ; Humans ; Leukocytes, Mononuclear/drug effects
Language	English
Publishing date	2019-03-06
Publishing country	Netherlands
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2727833-5
ISSN	1388-2139 ; 1383-5742
ISSN (online)	1388-2139
ISSN	1383-5742
DOI	10.1016/j.mrrev.2019.03.002
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Article: Interaction between dietary acrylamide intake and genetic variants for estrogen receptor-positive breast cancer risk

Hogervorst, Janneke G. F / van den Brandt, Piet A / Godschalk, Roger W. L / van Schooten, Frederik-Jan / Schouten, Leo J

European journal of nutrition. 2019 Apr., v. 58, no. 3

2019

Abstract: PURPOSE: The association between dietary acrylamide intake and estrogen receptor-positive (ER+) breast cancer risk in epidemiological studies is inconsistent. By analyzing gene-acrylamide interactions for ER+ breast cancer risk, we aimed to clarify the ... ...

Abstract	PURPOSE: The association between dietary acrylamide intake and estrogen receptor-positive (ER+) breast cancer risk in epidemiological studies is inconsistent. By analyzing gene-acrylamide interactions for ER+ breast cancer risk, we aimed to clarify the role of acrylamide intake in ER+ breast cancer etiology. METHODS: The prospective Netherlands Cohort Study on diet and cancer includes 62,573 women, aged 55–69 years. At baseline, a random subcohort of 2589 women was sampled from the total cohort for a case–cohort analysis approach. Dietary acrylamide intake of subcohort members (n = 1449) and ER+ breast cancer cases (n = 844) was assessed with a food frequency questionnaire. We genotyped single nucleotide polymorphisms (SNPs) in genes in acrylamide metabolism, sex steroid systems, oxidative stress and DNA repair. Multiplicative interaction between acrylamide intake and SNPs was assessed with Cox proportional hazards analysis, based on 20.3 years of follow-up. RESULTS: Unexpectedly, there was a statistically non-significant inverse association between acrylamide and ER+ breast cancer risk among all women but with no clear dose–response relationship, and no association among never smokers. Among the results for 57 SNPs and 2 gene deletions, rs1056827 in CYP1B1, rs2959008 and rs7173655 in CYP11A1, the GSTT1 gene deletion, and rs1052133 in hOGG1 showed a statistically significant interaction with acrylamide intake for ER+ breast cancer risk. CONCLUSIONS: This study did not provide evidence for a positive association between acrylamide intake and ER+ breast cancer risk. If anything, acrylamide was associated with a decreased ER+ breast cancer risk. The interaction with SNPs in CYP1B1 and CYP11A1 suggests that acrylamide may influence ER+ breast cancer risk through sex hormone pathways.
Keywords	DNA repair ; acrylamides ; breast neoplasms ; cohort studies ; dietary exposure ; dose response ; estrogens ; etiology ; food frequency questionnaires ; gene deletion ; genes ; genetic variation ; genotyping ; metabolism ; nutrition-genotype interaction ; oxidative stress ; single nucleotide polymorphism ; women ; Netherlands
Language	English
Dates of publication	2019-04
Size	p. 1033-1045.
Publishing place	Springer Berlin Heidelberg
Document type	Article
ZDB-ID	1466536-0
ISSN	1436-6215 ; 1436-6207
ISSN (online)	1436-6215
ISSN	1436-6207
DOI	10.1007/s00394-018-1619-z
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Article ; Online: Interaction between dietary acrylamide intake and genetic variants for estrogen receptor-positive breast cancer risk.

Hogervorst, Janneke G F / van den Brandt, Piet A / Godschalk, Roger W L / van Schooten, Frederik-Jan / Schouten, Leo J

European journal of nutrition

2018 Volume 58, Issue 3, Page(s) 1033–1045

Abstract: Purpose: The association between dietary acrylamide intake and estrogen receptor-positive (ER+) breast cancer risk in epidemiological studies is inconsistent. By analyzing gene-acrylamide interactions for ER+ breast cancer risk, we aimed to clarify the ... ...

Abstract	Purpose: The association between dietary acrylamide intake and estrogen receptor-positive (ER+) breast cancer risk in epidemiological studies is inconsistent. By analyzing gene-acrylamide interactions for ER+ breast cancer risk, we aimed to clarify the role of acrylamide intake in ER+ breast cancer etiology. Methods: The prospective Netherlands Cohort Study on diet and cancer includes 62,573 women, aged 55-69 years. At baseline, a random subcohort of 2589 women was sampled from the total cohort for a case-cohort analysis approach. Dietary acrylamide intake of subcohort members (n = 1449) and ER+ breast cancer cases (n = 844) was assessed with a food frequency questionnaire. We genotyped single nucleotide polymorphisms (SNPs) in genes in acrylamide metabolism, sex steroid systems, oxidative stress and DNA repair. Multiplicative interaction between acrylamide intake and SNPs was assessed with Cox proportional hazards analysis, based on 20.3 years of follow-up. Results: Unexpectedly, there was a statistically non-significant inverse association between acrylamide and ER+ breast cancer risk among all women but with no clear dose-response relationship, and no association among never smokers. Among the results for 57 SNPs and 2 gene deletions, rs1056827 in CYP1B1, rs2959008 and rs7173655 in CYP11A1, the GSTT1 gene deletion, and rs1052133 in hOGG1 showed a statistically significant interaction with acrylamide intake for ER+ breast cancer risk. Conclusions: This study did not provide evidence for a positive association between acrylamide intake and ER+ breast cancer risk. If anything, acrylamide was associated with a decreased ER+ breast cancer risk. The interaction with SNPs in CYP1B1 and CYP11A1 suggests that acrylamide may influence ER+ breast cancer risk through sex hormone pathways.
MeSH term(s)	Acrylamide/administration & dosage ; Acrylamide/adverse effects ; Aged ; Breast Neoplasms/epidemiology ; Breast Neoplasms/metabolism ; Cohort Studies ; Diet/methods ; Female ; Follow-Up Studies ; Genetic Variation/drug effects ; Humans ; Middle Aged ; Netherlands/epidemiology ; Polymorphism, Single Nucleotide/drug effects ; Prospective Studies ; Receptors, Estrogen ; Risk Factors ; Surveys and Questionnaires
Chemical Substances	Receptors, Estrogen ; Acrylamide (20R035KLCI)
Language	English
Publishing date	2018-02-14
Publishing country	Germany
Document type	Journal Article
ZDB-ID	1466536-0
ISSN	1436-6215 ; 1436-6207
ISSN (online)	1436-6215
ISSN	1436-6207
DOI	10.1007/s00394-018-1619-z
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Article ; Online: Bulky DNA adduct levels in normal-appearing colon mucosa, and the prevalence of colorectal adenomas.

Ho, Vikki / Peacock, Sarah / Massey, Thomas E / Godschalk, Roger W / van Schooten, Frederik J / Ashbury, Janet E / Vanner, Stephen J / King, Will D

Biomarkers : biochemical indicators of exposure, response, and susceptibility to chemicals

2018 Volume 23, Issue 8, Page(s) 735–741

Abstract: Purpose: Examine the association between bulky DNA adduct levels in colon mucosa and colorectal adenoma prevalence, and explore the correlation between adduct levels in leukocytes and colon tissue.: Methods: Bulky DNA adduct levels were measured ... ...

Abstract	Purpose: Examine the association between bulky DNA adduct levels in colon mucosa and colorectal adenoma prevalence, and explore the correlation between adduct levels in leukocytes and colon tissue. Methods: Bulky DNA adduct levels were measured using Results: An interaction between bulky DNA adduct levels and XPA rs1800975 on prevalence of colorectal adenoma was observed. Among individuals with lower DNA repair activity, increased DNA adduct levels were associated with increased colorectal adenoma prevalence (OR = 1.41 per SD increase, 95%CI: 0.92-2.18). Conversely, among individuals with normal DNA activity, an inverse association was observed (OR = 0.60 per SD increase, 95%CI: 0.34-1.07). Blood and colon DNA adduct levels were inversely correlated (ρ = -0.20). Conclusions: Among genetically susceptible individuals, higher bulky DNA adducts in the colon was associated with the prevalence of colorectal adenomas. The inverse correlation between blood and colon tissue measures demonstrates the importance of quantifying biomarkers in target tissues.
MeSH term(s)	Adenoma/etiology ; Adult ; Colorectal Neoplasms/etiology ; DNA Adducts/analysis ; Female ; Genetic Predisposition to Disease ; Humans ; Intestinal Mucosa/chemistry ; Male ; Middle Aged ; Polymorphism, Genetic ; Prevalence ; Xeroderma Pigmentosum Group A Protein/genetics
Chemical Substances	DNA Adducts ; XPA protein, human ; Xeroderma Pigmentosum Group A Protein
Language	English
Publishing date	2018-07-23
Publishing country	England
Document type	Journal Article
ZDB-ID	1324372-x
ISSN	1366-5804 ; 1354-750X
ISSN (online)	1366-5804
ISSN	1354-750X
DOI	10.1080/1354750X.2018.1485055
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