Chemical, Physical, and Genetic Factors Interfering with DNA Repair-a Review
Identifieur interne : 003675 ( Main/Exploration ); précédent : 003674; suivant : 003676Chemical, Physical, and Genetic Factors Interfering with DNA Repair-a Review
Auteurs : Naomi Jean Bernheim ; Hans FalkSource :
- International Journal of Toxicology [ 1091-5818 ] ; 1983-05.
English descriptors
- Teeft :
- Aberration, Acad, Academic press, Acridine, Acriflavine, Acta, Adriamycin, Aflatoxin, Alkylating, Alkylating agents, Arsenite, Ataxia, Ataxia telangiectasia, Ataxia telangiectasia cells, Bernheim, Biochem, Biol, Biophys, Bleomycin, Caffeine, Cancer inst, Carcinogen, Carcinogenesis, Cell death, Chemical carcinogens, Chinese hamster cells, Chromosomal, Chromosomal aberrations, Chromosome, Chromosome aberrations, Chromosome damage, Chromosome repair, Cleaver, Cockayne syndrome, Coli, Commun, Cycloheximide, Deoxyribonucleic acid, Derivative, Dimer, Energy metabolism, Enhancement, Enzymatic removal, Excision, Excision repair, Excision repair enzymes, Faba, Falk, Fibroblast, Friedberg, Genetic diseases, Genetic effects, Gyrase, Hamster, Hanawalt, Harman, Hela, Hela cells, Human cells, Human diseases, Human fibroblasts, Human lymphocytes, Hydrazide, Hydroxyurea, Hyperthermia, Inhibition, Inhibitor, Kaplan, Kihlman, Lesion, Lethal damage, Ligase, Lymphocyte, Maher, Mammalian, Mammalian cells, Methanesulfonate, Methyl, Methylated oxypurines, Mitomycin, Moroson, Mutagen, Mutagenic, Mutant, Mutat, Mutation, Nalidixic, Nalidixic acid, Natl, Nitrosoureas, Novobiocin, Nucleic acids, Nucleotide, Partial inhibition, Paterson, Pathway, Pegg, Physical agents, Pigmentosum, Polymerase, Postreplication repair, Potassium cyanide, Precursor, Proc, Proc natl, Prokaryote, Protein synthesis, Protein synthesis inhibition, Purine, Puromycin, Pyrimidine, Quinacrine, Radiat, Radiat biol, Regan, Repair, Repair enzymes, Repair inhibition, Repair inhibitor, Repair inhibitors, Repair mechanism, Repair mechanisms, Repair process, Repair processes, Repair replication, Repair synthesis, Repair system, Repair systems, Replication, Semiconservative, Semiconservative replication, Setlow, Single strand breaks, Singlestrand breaks, Sodium arsenite, Stich, Strand breaks, Telangiectasia, Ultraviolet light, Ultraviolet radiation, Unscheduled, Xeroderma, Xeroderma pigmentosum, Xeroderma pigmentosum cells.
Abstract
Because of its function as transmitter of genetic information, DNA is the most important macromolecule in need of protection from attack by chemical and physical agents, but mechanisms have evolved for repairing such damage to DNA. The presence of the adaptive response and other cellular repair systems (excision, post-replication, SOS, etc.) diminishes the toxicologic effects of low doses of toxic or muta-genic substances. Whether or not these genotoxic effects can be reduced to undetectable levels is not certain. Nonetheless, this repair-mediated diminution of damage due to chemicals constitutes one of the arguments in favor of existence of “safe” threshold levels of chemical exposure (Schendel, 1981). In turn, the repair process itself may be affected by chemical and physical agents. To determine the mode of action of a specific compound on the process of DNA repair becomes complex when all factors are taken into consideration. There are agents which interfere with DNA repair but they are also as active or more active in suppressing replicative DNA synthesis, as well as RNA and protein synthesis. The interference with repair may arise from other major processes such as alteration of energy metabolism and effects on precursor pathways and/or enzymatic cofactors. Whether or not an agent can specifically inhibit DNA repair enzymes has not been answered. The point must be made, however, that this type of interference with essential protective mechanisms is taking place and it may change anticipated outcomes of chemical or physical exposures. The magnitude of this effect due to the exposure of people to so many chemicals should be recognized and studied for their degree of interference with all the processes of DNA repair.
Url:
DOI: 10.3109/10915818309140690
Affiliations:
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first="Hans" last="Falk">Hans Falk</name><affiliation><wicri:noCountry code="no comma">National Institute of Environmental Health Sciences</wicri:noCountry></affiliation></author></analytic><monogr></monogr><series><title level="j">International Journal of Toxicology</title><idno type="ISSN">1091-5818</idno><idno type="eISSN">1092-874X</idno><imprint><publisher>SAGE Publications</publisher><pubPlace>Sage CA: Los Angeles, CA</pubPlace><date type="published" when="1983-05">1983-05</date><biblScope unit="volume">2</biblScope><biblScope unit="issue">3</biblScope><biblScope unit="page" from="23">23</biblScope><biblScope unit="page" to="54">54</biblScope></imprint><idno type="ISSN">1091-5818</idno></series></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">1091-5818</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="Teeft" xml:lang="en"><term>Aberration</term><term>Acad</term><term>Academic press</term><term>Acridine</term><term>Acriflavine</term><term>Acta</term><term>Adriamycin</term><term>Aflatoxin</term><term>Alkylating</term><term>Alkylating agents</term><term>Arsenite</term><term>Ataxia</term><term>Ataxia telangiectasia</term><term>Ataxia telangiectasia cells</term><term>Bernheim</term><term>Biochem</term><term>Biol</term><term>Biophys</term><term>Bleomycin</term><term>Caffeine</term><term>Cancer inst</term><term>Carcinogen</term><term>Carcinogenesis</term><term>Cell death</term><term>Chemical carcinogens</term><term>Chinese hamster cells</term><term>Chromosomal</term><term>Chromosomal aberrations</term><term>Chromosome</term><term>Chromosome aberrations</term><term>Chromosome damage</term><term>Chromosome repair</term><term>Cleaver</term><term>Cockayne syndrome</term><term>Coli</term><term>Commun</term><term>Cycloheximide</term><term>Deoxyribonucleic acid</term><term>Derivative</term><term>Dimer</term><term>Energy metabolism</term><term>Enhancement</term><term>Enzymatic removal</term><term>Excision</term><term>Excision repair</term><term>Excision repair enzymes</term><term>Faba</term><term>Falk</term><term>Fibroblast</term><term>Friedberg</term><term>Genetic diseases</term><term>Genetic effects</term><term>Gyrase</term><term>Hamster</term><term>Hanawalt</term><term>Harman</term><term>Hela</term><term>Hela cells</term><term>Human cells</term><term>Human diseases</term><term>Human fibroblasts</term><term>Human lymphocytes</term><term>Hydrazide</term><term>Hydroxyurea</term><term>Hyperthermia</term><term>Inhibition</term><term>Inhibitor</term><term>Kaplan</term><term>Kihlman</term><term>Lesion</term><term>Lethal damage</term><term>Ligase</term><term>Lymphocyte</term><term>Maher</term><term>Mammalian</term><term>Mammalian cells</term><term>Methanesulfonate</term><term>Methyl</term><term>Methylated oxypurines</term><term>Mitomycin</term><term>Moroson</term><term>Mutagen</term><term>Mutagenic</term><term>Mutant</term><term>Mutat</term><term>Mutation</term><term>Nalidixic</term><term>Nalidixic acid</term><term>Natl</term><term>Nitrosoureas</term><term>Novobiocin</term><term>Nucleic acids</term><term>Nucleotide</term><term>Partial inhibition</term><term>Paterson</term><term>Pathway</term><term>Pegg</term><term>Physical agents</term><term>Pigmentosum</term><term>Polymerase</term><term>Postreplication repair</term><term>Potassium cyanide</term><term>Precursor</term><term>Proc</term><term>Proc natl</term><term>Prokaryote</term><term>Protein synthesis</term><term>Protein synthesis inhibition</term><term>Purine</term><term>Puromycin</term><term>Pyrimidine</term><term>Quinacrine</term><term>Radiat</term><term>Radiat biol</term><term>Regan</term><term>Repair</term><term>Repair enzymes</term><term>Repair inhibition</term><term>Repair inhibitor</term><term>Repair inhibitors</term><term>Repair mechanism</term><term>Repair mechanisms</term><term>Repair process</term><term>Repair processes</term><term>Repair replication</term><term>Repair synthesis</term><term>Repair system</term><term>Repair systems</term><term>Replication</term><term>Semiconservative</term><term>Semiconservative replication</term><term>Setlow</term><term>Single strand breaks</term><term>Singlestrand breaks</term><term>Sodium arsenite</term><term>Stich</term><term>Strand breaks</term><term>Telangiectasia</term><term>Ultraviolet light</term><term>Ultraviolet radiation</term><term>Unscheduled</term><term>Xeroderma</term><term>Xeroderma pigmentosum</term><term>Xeroderma pigmentosum cells</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Because of its function as transmitter of genetic information, DNA is the most important macromolecule in need of protection from attack by chemical and physical agents, but mechanisms have evolved for repairing such damage to DNA. The presence of the adaptive response and other cellular repair systems (excision, post-replication, SOS, etc.) diminishes the toxicologic effects of low doses of toxic or muta-genic substances. Whether or not these genotoxic effects can be reduced to undetectable levels is not certain. Nonetheless, this repair-mediated diminution of damage due to chemicals constitutes one of the arguments in favor of existence of “safe” threshold levels of chemical exposure (Schendel, 1981). In turn, the repair process itself may be affected by chemical and physical agents. To determine the mode of action of a specific compound on the process of DNA repair becomes complex when all factors are taken into consideration. There are agents which interfere with DNA repair but they are also as active or more active in suppressing replicative DNA synthesis, as well as RNA and protein synthesis. The interference with repair may arise from other major processes such as alteration of energy metabolism and effects on precursor pathways and/or enzymatic cofactors. Whether or not an agent can specifically inhibit DNA repair enzymes has not been answered. The point must be made, however, that this type of interference with essential protective mechanisms is taking place and it may change anticipated outcomes of chemical or physical exposures. The magnitude of this effect due to the exposure of people to so many chemicals should be recognized and studied for their degree of interference with all the processes of DNA repair.</div></front></TEI><affiliations><list></list><tree><noCountry><name sortKey="Bernheim, Naomi Jean" sort="Bernheim, Naomi Jean" uniqKey="Bernheim N" first="Naomi Jean" last="Bernheim">Naomi Jean Bernheim</name><name sortKey="Falk, Hans" sort="Falk, Hans" uniqKey="Falk H" first="Hans" last="Falk">Hans Falk</name></noCountry></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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