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DNA Adducts: Endogenous and Induced [PDF]

open access: possibleToxicologic Pathology, 2000
Human exposure to DNA damaging agents can arise from exogenous sources or endogenous processes that occur normally or in pathological states. DNA isolated from human tissues, obtained from the very young to the old, contains detectable amounts of a number of different types of DNA adducts that reflect exposure to both known carcinogens and as yet ...
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Measurement of DNA Adducts by Immunoassays

1990
The ability to monitor for chemical carcinogen-DNA adducts in human tissues provides an indication that human exposure has occurred. Such data may eventually demonstrate the dose received and/or allow the prediction of cancer risk. At the present time evidence that the occurrence of certain adducts is associated with specific chemical exposures is ...
Eddie Reed   +3 more
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Identification of DNA Adducts of Acetaldehyde

Chemical Research in Toxicology, 2000
Acetaldehyde is a mutagen and carcinogen which occurs widely in the human environment, sometimes in considerable amounts, but little is known about its reactions with DNA. In this study, we identified three new types of stable acetaldehyde DNA adducts, including an interstrand cross-link.
Edward J. McIntee   +5 more
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Correlation of DNA adduct levels with tumor incidence: carcinogenic potency of DNA adducts

Mutation Research/Fundamental and Molecular Mechanisms of Mutagenesis, 1999
The quantitative relationship between DNA adducts and tumor incidence is evaluated in this review. All available data on DNA adduct levels determined after repeated administration of a carcinogen to rats or mice have been compiled. The list comprised 27 chemicals, of all major structural classes of carcinogens. For the correlation with tumor incidence,
Michael Otteneder, Werner K. Lutz
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DNA Adducts and Carcinogenesis

1989
A central tenet of cancer research is that tumors arise from cells that have undergone a permanent heritable change in their genetic material. This hypothesis originated from the observation that tumor cells have lost normal growth-control mechanisms and transmit this characteristic to their progeny. It is supported by the findings that most chemically
Miriam C. Poirier, Frederick A. Beland
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[7] Copper-DNA adducts

1994
Publisher Summary Redox active metal ions, such as iron and copper play a central role in the formation of reactive oxygen species in biological systems. Although iron has received the most attention in this capacity, the role of copper may be particularly crucial because copper occurs naturally in chromosomes, where it is believed to play a role in ...
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DNA adduct assay in cervical epithelium [PDF]

open access: possibleDiagnostic Cytopathology, 1994
AbstractNumerous epidemiological studies have shown that there is an association between smoking and cervical cancer. However, the essential evidence to show whether this relationship is casual or causal is lacking. The demonstration of DNA modification by tobacco components in the cervical epithelium would provide biochemical evidence to support a ...
David H. Phillips   +2 more
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Control of DNA Hybridization with Photocleavable Adducts

Photochemistry and Photobiology, 2005
ABSTRACTPrevious reports have shown that 1‐(4,5‐dimethoxy‐2‐nitro‐phenyl)ethyl ester (DMNPE) adducts coupled to DNA plasmids block transcription in vitro and in vivo until removed with light. In this report, we explore the use of DMNPE to control DNA hybridization.
W. Todd Monroe   +3 more
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The 32P-postlabeling assay for DNA adducts [PDF]

open access: possibleNature Protocols, 2007
32P-postlabeling analysis is an ultrasensitive method for the detection and quantitation of carcinogen-DNA adducts. It consists of four principal steps: (i) enzymatic digestion of DNA to nucleoside 3'-monophosphates; (ii) enrichment of the adduct fraction of the DNA digest; (iii) 5'-labeling of the adducts by transfer of 32P-orthophosphate from [gamma ...
Phillips, David H, Arlt, Volker M
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DNA adducts and cell cycle

Journal of Cancer Research and Clinical Oncology, 1986
Cell cycle-dependent differences of transformation sensitivity may be due to alterations in the formation of ultimate electrophilic carcinogens during the cell cycle, preferential primary adduct formation during specific phases of the cell cycle, e.g. binding to single stranded DNA at the replication fork, base-mispairing and mutation of transformation-
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