Mechanisms of resistance to xenobiotics in human therapy
Identifieur interne : 002809 ( Main/Exploration ); précédent : 002808; suivant : 002810Mechanisms of resistance to xenobiotics in human therapy
Auteurs : I. Saves ; J.-M. MassonSource :
- Cellular and Molecular Life Sciences CMLS [ 1420-682X ] ; 1998-05-01.
English descriptors
Abstract
Abstract.: Xenobiotic resistance is the major cause of failure in human therapies. Because of their serious clinical and economical consequences, resistance phenomena have been intensively studied in the case of antibacterial, anticancer, antipaludic and anti-human immunodeficiency virus-1 therapies. Beside pharmacological factors that can impede the action of the drugs, several cellular mechanisms of resistance have been described. Surprisingly, these mechanisms are conserved among bacteria, eucaryotic cells, parasites and viruses. The efficiency of drugs can be circumvented by alteration of the drug cellular concentration (altered influx, enhanced efflux or sequestration), detoxification, alteration of the drug target, nonactivation or inactivation of the drug, or by enhanced DNA repair.
Url:
DOI: 10.1007/s000180050170
Affiliations:
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Le document en format XML
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<front><div type="abstract" xml:lang="en">Abstract.: Xenobiotic resistance is the major cause of failure in human therapies. Because of their serious clinical and economical consequences, resistance phenomena have been intensively studied in the case of antibacterial, anticancer, antipaludic and anti-human immunodeficiency virus-1 therapies. Beside pharmacological factors that can impede the action of the drugs, several cellular mechanisms of resistance have been described. Surprisingly, these mechanisms are conserved among bacteria, eucaryotic cells, parasites and viruses. The efficiency of drugs can be circumvented by alteration of the drug cellular concentration (altered influx, enhanced efflux or sequestration), detoxification, alteration of the drug target, nonactivation or inactivation of the drug, or by enhanced DNA repair.</div>
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