Esterases resistance mechanisms

Organophosphate resistance in M. persicae is due to the production of large amounts of carboxylesterase E4 that degrade as well as sequester these insecticides (12). This is believed to be the only biochemical resistance mechanism in this species in many countries, including the UK., continental Europe, Japan, and Australia (25.). E4 additionally confers low levels of resistance to carbamates and to (IS)-trans-permethrin (12). This esterase has been characterized extensively by toxicological, biochemical, immunological and molecular studies (2, 22, 22f 22, 22) ... 

The mechanisms of resistance fall into two main categories. Many insects produce an increased level of detoxifying enzymes, such as esterases, that modify the insecticides to inactive metabolites very rapidly. Such a system is seen in aphids that are resistant to OP insecticides. In other cases it is the target site that is modified such that the insecticide (the enzyme inhibitor) no longer binds to the target and is, therefore, ineffective. This has recently been shown to occur in some aphids that are resistant to OP insecticides but the classical example is knockdown resistance (kdr) and super-kdr to pyrethroid insecticides shown by many insects but particularly house flies Musca domes tied). This resistance is thought to result from a modification of... 

Resistance to erythromycin is becoming a serious clinical problem. For example, most strains of staphylococci in hospital isolates are resistant to this drug. Several mechanisms have been identified (1) the inability of the organism to take up the antibiotic (2) a decreased affinity of the 50S ribosomal subunit for the antibiotic resulting from the methylation of an adenine of the 23S bacterial ribosomal RNA and (3) presence of a plasmid-associated erythromycin esterase. Both clarithromycin and azithromycin show cross-resistance with erythromycin. 

The routine use of the macrolides is limited because bacterial resistance develops quickly following repeated exposure. There can be crossresistance between the drugs in this class. The mechanisms of resistance include decreased drug entry into bacteria, inability to bind to the SOS ribosomal subunit and the plasmid-mediated production of macrolide-destroying esterase. 

Herbert Oberlander coordinated the section that features chapters on sac-specific selection using chimeric genes potential applications of neuroendocrine research to insect control insect cuticle structure and metabolism molecular aspects of immune mechanisms in insects molecular genetics of nerve insensitivity resistance to insecticides and inhibition of juvenile hormone esterase by transition-state analogs. 

Esterasss. Esterases are a major mechanism of resistance to organophosphates and in certain cases may also contribute resistance toward carbamates and certain pyrethroids. The role of esterases in resistance in mosquitoes and aphids has been the subject of especially fruitful research during the past few years. In collaborative studies between our laboratory and French laboratories in Montpellier, Antibes and Pau, several electrophoretic forms of esterases A and B have been identified in mosquitoes (Figure 5). Esterases Ai, A2, A4, Bi, B2, and B4 are found in the Culex pipiens complex, i.e. C. pipiens and C. quinquefasciatus. Two other forms, esterases A3 and B3, are present in C. tarsalis, and still others (not yet named) in Aedes aegypti and Ae. nigromaculis from California, C. tritaeniorhynchus from Japan (22) and various Culex species from Mexico. 

Resistance to macrolides can result from (1) drug efflux by an active pump mechanism (2) ribosomal protection by inducible or constitutive production of methylase enzymes that modify the ribosomal target and decrease drug binding (3) macrolide hydrolysis by esterases produced by Enterobacteriaceae and (4) chromosomal mutations that alter a SOS ribosomal protein (found in B. subtilis, Campylobacter spp., mycobacteria, and gram-positive cocci). 

Esterase formation is a mechanism of macrolide resistance seen in coliforms. Resistance to tetracyclines occurs either from increased activity of efflux mechanisms or changes in cell membrane permeability, leading to decreases in intracellular levels of such drugs. Resistance to chloramphenicol involves plasmid-mediated formation of drug-inactivating acetyltrans-ferases. The answer is (A). 

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