2 edition of Repair of DNA lesions introduced by N-nitroso compounds found in the catalog.
Repair of DNA lesions introduced by N-nitroso compounds
1986 by Norwegian University Press, Distributed world-wide excluding Scandinavia by Oxford University Press in Oslo, Oxford, New York .
Written in English
Includes bibliographies and indexes.
|Statement||edited by Bjørnar Myrnes and Hans Krokan.|
|Contributions||Myrnes, Bjørnar., Krokan, Hans.|
|LC Classifications||QH467 .R46 1986|
|The Physical Object|
|Pagination||292 p. :|
|Number of Pages||292|
|LC Control Number||86193085|
Thirty-day-old Sprague--Dawley rats were used to study the persistence of DNA lesions (e.g., O6-alkylguanine) induced by various doses of ethylnitrosourea (ENU). Cellular proliferation was measured as an increment of DNA content per organ at 7 days post-treatment. Clapp R et al; N-Nitroso Compounds. Patty's Toxicology. 6th ed. ( IN: ACS Symposium Series , Nitrosamines and Related N-Nitroso Compounds: Chemistry and Biochemistry, p Olken N.M., Osowa Y., Marletta M.A. Characterization of the inactivation of nitric oxide by NG-methyl-L-arginine: evidence for heme loss.
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Repair of DNA lesions introduced by N-nitroso compounds. Oslo: Norwegian University Press ; Oxford ; New York: Distributed world-wide excluding Scandinavia by Oxford University Press, © (OCoLC) Document Type: Book: All Authors / Contributors: Bjørnar Myrnes; Hans Krokan.
Depurination of guanines (or adenines) is a common DNA lesion. Three of the four DNA bases, adenine, guanine, and cytosine, contain amine groups that can be lost in a variety of pH and temperature-dependent reactions that convert the bases to hypoxanthine, xanthine, and uracil, respectively.
particularly Repair of DNA lesions introduced by N-nitroso compounds book compounds, are formed in. We found that, in Escherichia coli cells, these lesions mildly (O 6-POB-dG), moderately (O 6-PHB-dG), or strongly (O 6-CM-dG, O 6-ACM-dG, and O 6-HOEt-dG) impede DNA replication. The strong blockage effects of the last three lesions were attributable to the presence of hydrogen-bonding donor(s) located on the alkyl functionality of these by: 2.
Repair-Resistant DNA Lesions Nicholas E. Geacintov* and Suse Broyde Chemistry and Biology Departments, New York University, New York, New YorkUnited States ABSTRACT: The eukaryotic global genomic nucleotide excision repair (GG-NER) pathway is the major mechanism that removes most bulky and some nonbulky lesions from cellular DNA.
The BER pathway is crucial for the repair of the main N-alkylation DNA adducts, in particular N3-methyladenine, N3-methylguanine and N7-methylguanine, which is mediated in the first step of the pathway by the alkyladenine-DNA glycosylase (AAG; also designated as N -methylpurine-DNA glycosylase) (34–36).Cited by: Methylated pyrimidine lesions in the DNA of mammalian cells, in Repair of DNA lesions introduced by N-nitroso compounds, eds.
Krokan and R. Myrnes. Oxford University Press, in press. ties of selected DNA lesions, and how the lesions are processed by the DNA repair, replication, and transcription machineries.
The chemistry of DNA damage is complex and the variety of DNA lesions is enormous. This book considers an important subset of DNA lesions that illustrate. The relative importance of DNA replication, DNA repair and metabolic activation in induction of cancer by N-nitroso compounds Norwegian University Press Oslo 9 Challen C.
Lunec J. Warren W. Collier J. Bassendine MF. DNA synthesis) Interstrand cross-links, Double-strand DNA breaks Total damage from all mechanisms: - lesions/day.
Diverse DNA repair systems • Augment DNA polymerase proofreading • Mostly characterized in bacteria • General mechanisms shared in eukaryotes 1.
Direct repair, e.g. pyrimidine dimers 2. Base excision repair 3. DNA replication studies of N-nitroso compound–induced O 6-alkyl-2′-deoxyguanosine lesions in Escherichia coli. Pengcheng Wang 1, SOS-induced DNA polymerases played redundant roles in bypassing all the O 6-alkyl-dG lesions investigated.
DNA polymerase IV (Pol IV) and Pol V. They tested 19 anti-oxidant compounds and of these 19 compounds only chlorogenic acid and its metabolic products: chlorogenic acid, caffeic acid, m-coumaric acid and 3-(m-hydroxyphenyl) propionic acid, increased expression of the two tested DNA repair genes in HCT cells (Table 10).
Hemoglobin Adducts, DNA Adducts, and Urinary Metabolites of Tobacco-Specific Nitrosamines N-NITROSO COMPOUND FORMATION AND INHIBITION: BRIEF DISCUSSIONS OF RESEARCH. Nitrosamide Formation from Foodstuffs.
(Acetoxymethylnitrosamino)(3-pyridyl)butanone Inhibits the Repair of O6-Methylguanine. Lisa A. Peterson, Xiao-Keng Liu, and. Potential human exposures to N-nitroso compounds occur not only environmentally, but also from their synthesis in vivo.
DNA alkylation by N-nitroso compounds involves formation of reactive alkyldiazonium ions, which result from decomposition of N-alkyl-N-nitrosoureas and N-alkyl-N′-nitro-N-nitrosoguanidines (Margison and O’Connor ). 3 Common themes in all DNA repair pathways: Detection of the lesion: protein or proteins that specifically detect and bind the particular DNA lesion Removal of the damaged DNA: glycosylases, nucleases, etc Resynthesis/Repair: DNA polymerases, DNA ligases Regulatory proteins: protein kinases etc Effects on other cellular processes.
This book attempts to demonstrate the complexity of the mechanisms of biological action of the toxic N-nitroso compounds. The conclusions presented on genetic toxicology are based on comparative studies of biological assays and a firm foundation of chemical structural relations among N-nitroso compounds.
of DNA damage and mutation or a decrease of DNA repair. Deficient DNA repair cause tissue degeneration and premature ageing is indicated by number of human genetic defects such as CS and XP. XP patients having skin and eye photosensitivity exhibit premature cutaneous ageing, increased incidence of basal cell carcinoma and melanoma.
The relationships between DNA alkylation, DNA repair and mutagenesis by N-nitroso compounds in Salmonella were examined. DNA adducts formed by treatment of the bacteria with N-nitroso compounds were monitored. Critical to the study was establishing which adducts led to mutations.
Two methods were employed. are caused by DNA repair deﬁciencies . In this chapter the major types of DNA damage and the respective molecular pathways that function in their repair will be introduced (see Fig.
Types of DNA Damage As a prelude to the repair of damaged DNA, we must ﬁrst take into consideration the collection of damage products. DNA repair mechanisms are critical for maintaining the integrity of genomic DNA, and their loss is associated with cancer predisposition syndromes.
Studies in Saccharomyces cerevisiae have played a central role in elucidating the highly conserved mechanisms that promote eukaryotic genome stability. This review will focus on repair mechanisms that involve excision of a single strand from.
Alkylation of DNA at theO 6 position of guanine is regarded as one of the most critical events leading to induction of mutations and cancers in organisms. OnceO 6-methylguanine is formed, it can pair with thymine during DNA replication, the result being a conversion of the guanine cytosine to an adeninethymine pair in DNA, and such mutations are often found in tumors induced by alkylating.
The DNA molecule is chemically unstable giving rise to DNA lesions of different nature. That is why DNA damage detection, signaling and repair, collectively known as the DNA. RNA polymerase transcribes DNA normally until it reaches the lesion in DNA. (RNAp stalls and txn stops) RNAp recruits nucleotide excision repair proteins to the site of the lesion, and the RNAp either backup or dissociates from the lesion to allow the repair proteins to access the lesion.
The eukaryotic global genomic nucleotide excision repair (GG-NER) pathway is the major mechanism that removes most bulky and some nonbulky lesions from cellular DNA. There is growing evidence that certain DNA lesions are repaired slowly or are entirely resistant to repair in cells, tissues, and in cell extract model assay systems.
Mutation and Repair of DNA Damages Induced by Nitroaromatic Compounds. structure and conformation of the lesion, (ii) DNA sequence context, (iii) the type of cell in which it is replicated, (iv) whether or not the cells were induced for certain functions (e.g., SOS), and (v) the repair status of the cell.
Adducts or lesions in DNA by. Download Bones Brains And Dna Book For Free in PDF, EPUB. In order to read online Bones Brains And Dna textbook, you need to create a FREE account.
Read as many books as you like (Personal use) and Join Over Happy Readers. We cannot guarantee that every book is in the library. DNA repair is regulated in mammalian cells by a sensing mechanism that detects DNA damage and activates a protein called p p53 is a transcriptional regulatory factor that controls the expression of some gene products that affect cell cycling, DNA replication and DNA repair.
DNA repair is a collection of processes by which a cell identifies and corrects damage to the DNA molecules that encode its genome. In human cells, both normal metabolic activities and environmental factors such as radiation can cause DNA damage, resulting in as many as 1 million individual molecular lesions per cell per day.
Many of these lesions cause structural damage to the DNA molecule. DNA repair begins when the xeroderma pigmentosum C protein complex (XPC) patrols the genome for certain types of DNA lesions.
Upon encountering damaged DNA, it inserts a simple protein structure shaped like a hairpin between the two DNA strands so NER proteins can recognize the lesion. Transcription bypass of DNA lesions enhances cell survival but attenuates transcription coupled DNA repair.
Nucleic Acids Research42 (21), DOI: /nar/gku Kristin Limpose, Anita H Corbett, Paul W Doetsch. DNA Damage. DNA Repair Mechanisms PPT (Introduction to DNA Repair Mechanism PPT) What is DNA Repair.
DNA damaging agents, DNA ‘lesions’, Different DNA Repair Mechanisms in the cell, Noble Prize in Chemistry.
Learn more: DNA Repair Mechanism Video Tutorial. DNA Lesions are sites of damage in the base-pairing or structure of DNA. They are classified as follows: Abasic Site: This is where a base is missing from the DNA (note that the sugar-phosphate backbone is still intact, just the base is missing).This occurs due to a rise in temperature, a drop in pH, or the presence of alkylations on the base, that destabilize the N-glycosidic bonds.
Humans are exposed to N-nitroso compounds from both endogenous and exogenous N-nitroso compounds can be metabolically activated to give diazoacetate, which can result in the carboxymethylation of remarkable similarity in p53 mutations found in human gastrointestinal tumors and in shuttle vector studies, where the human p53 gene-containing vector was treated with.
The genome of a typical mammalian cell accumulates many thousands of lesions in a hour period. However, as a result of DNA repair, less than one lesion in 1, becomes a mutation. DNA is a relatively stable molecule, but without repair systems the cumulative effect of many infrequent but damaging reactions would make life impossible.
All. ÐLiving cells contain several DNA repair systems that can fix different type of DNA alterations. DNA repair mechanisms fall into 2 categories ÐRepair of damaged bases ÐRepair of incorrectly basepaired bases during replication.
In most cases, DNA repair is a multi-step process Ð1. An irregularity in DNA structure is detected Ð2. N-nitroso compounds involved working up a batch of material by preferential extraction, concentration of the extract and chromatographic identification of the N-nitroso compound in a particular band, often using a colour reagent.
As mentioned, the sensitivity of. In case of DNA instability, such as ataxia telangectesia, it is very difficult to promote DNA repair.
Under some conditions also a treatment with antioxidants may induce DNA repair. Cite. Long term persistence of nitrosamine-induced structural damage to heterochromatic DNA.
In H. Bartsch, I. O'Neil, & R. Schulte-Hermann (Eds.), Relevance of N-nitroso compounds to human cancer: Exposures and mechanisms. Paper presented at the International Symposium on N-nitroso Compounds, Baden, September (pp. DNA repair pathway is considered to be one of the most important mechanisms that protect cells from intrinsic and extrinsic stresses.
It has been established that DNA repair activity has a crucial role in the way that cancer cells respond to treatment. Sarcomas are a group of tumors with mesenchymal origin in which their association with DNA repair aberrations has been reported in numerous.
N-nitroso compounds result from reactions involving other chemicals called alkylamines. At room temperature, N-nitroso compounds are yellow liquids. They do not have a distinct odor.
Industry makes small amounts of N-nitroso compounds for research. They can also be formed as a side-reaction when other products are made. Formation. 6-O-Methylguanine is formed in DNA by alkylation of the oxygen atom of guanine, most often by N-nitroso compounds (NOC) and sometimes due to methylation by other compounds such as endogenous S-adenosyl are alkylating agents formed by the reaction of nitrite or other nitrogen oxides with secondary amines and N-alkylamides, yielding N-alkylnitrosamines and N.
Originally published inthis volume looks in depth at the carcinogenic properties of N-nitroso compounds. These compounds occur widely in smoked foods and in meat and fish cured with nitrates; they are also formed in some industrial processes and in addition are found in cosmetics, tobacco and tobacco smoke.
Mismatch repair enzymes recognize the wrongly incorporated base and excise it from the DNA, replacing it with the correct base. In yet another type of repair, nucleotide excision repair, the incorrect base is removed along with a few bases on the 5' and 3' end, and these are replaced by copying the template with the help of DNA polymerase.Bogden JM, Eastman A, Bresnick E.
A system in mouse liver for the repair of O6-methylguanine lesions in methylated DNA. Nucleic Acids Res. Jul 10; 9 (13)– [PMC free article] Pegg AE, Perry W. Stimulation of transfer of methyl groups from O6-methylguanine in DNA to protein by rat liver extracts in response to hepatotoxins.