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Esterases resistance

Like carbachol bethanechol is an esterase resistant quaternary ammonium compound which can be used for the same indications. [Pg.294]

Hofling K, Brossmta- R, Klenk H, Herrler G (1996) Transfer of an esterase-resistant receptor analog to the surface of influenza C virions results in reduced infectivity due to aggregate formation. Virology 218 127-133... [Pg.22]

Hydrolysis of macrolides by products of the ere genes detected in enterobacteria is only of scientific interest, while esterases VGB-A and VGB-B encoded by the vgb type genes mediate clinically relevant resistance in staphylococci to the B compound (quinupristin) of the streptogramin combination quinu-pristin-dalfopristin. [Pg.103]

Another group of antibiotics that can be inactivated by hydrolysis are 14- and 15- membered macrolides [2]. Esterases cleave the lactone ring. The plasmid encoded ere genes are found in members of the Enter-obacteriaceae and increase the intrinsic resistance. Furthermore, these esterases can also be found in some isolates of erythromycin resistant staphylococci. [Pg.771]

There are marked species differences in A-esterase activity. Birds have very low, often undetectable, levels of activity in plasma toward paraoxon, diazoxon, pirimi-phos-methyl oxon, and chlorpyrifos oxon (Brealey et al. 1980, Mackness et al. 1987, Walker et al. 1991 Figure 2.10). Mammals have much higher plasma A-esterase activities to all of these substrates. The toxicological implications of this are discussed in Chapter 10. Some species of insects have no measurable A-esterase activity, even in strains that have resistance to OPs (Mackness et al. 1982, Walker 1994). These include the peach potato aphid (Myzus persicae Devonshire 1991) and the... [Pg.37]

OPs Myzus persicae Resistant clones (85-315) Enhanced B esterase Multiple copies of gene... [Pg.94]

In addition to ester bonds with P (Section 10.2.1, Figures 10.1 and 10.2), some OPs have other ester bonds not involving P, which are readily broken by esteratic hydrolysis to bring about a loss of toxicity. Examples include the two carboxylester bonds of malathion, and the amido bond of dimethoate (Figure 10.2). The two carboxylester bonds of malathion can be cleaved by B-esterase attack, a conversion that provides the basis for the marked selectivity of this compound. Most insects lack an effective carboxylesterase, and for them malathion is highly toxic. Mammals and certain resistant insects, however, possess forms of carboxylesterase that rapidly hydrolyze these bonds, and are accordingly insensitive to malathion toxicity. [Pg.199]

Devonshire, A.L. (1991). Role of esterases in resistance of insects to insecticides. In Biochemical Society Transactions 19, 755-759. [Pg.344]

Carboxylesterases are well-represented in insects and are sometimes important in the development of resistance to insecticides. Thus, a well-characterized carboxylesterase E4 is responsible for resistance to organophosphorus insecticides in the aphid (Myzuspersicae) [107]. In the California Culex mosquito, the esterase B1 is 500-fold more abundant in organophosphate-resistant than in susceptible insects. The increase of esterase levels is the result of gene amplification, i.e., the resistant animals have an increased number of copies of the structural esterase gene [108],... [Pg.52]

L. M. Field, A. L. Devonshire, B. G. Forde, Molecular Evidence that Insecticide Resistance in Peach-Potato Aphids (Myzus persicae Sulz.) Results from Amplification of an Esterase Gene , Biochem. J. 1988, 257, 309-312. [Pg.63]

Through its structural similarity to acetylcholine (Figure 3.7b), muscarine binds to the acetylcholine receptor on the synapses of nerve endings of smooth muscles and endocrine glands, causing the well-known parasympaticomimetic effects. Because muscarine is not an ester like acetylcholine, and hence resists esterase activity, it is not degraded and so can cause continuous stimulation of the affected neurons. [Pg.85]

Resistance can occur via plasmid-mediated meth-ylation of the receptor site which reduces the binding of the macrolide. Also plasmid-mediated esterase activity, especially in coliform bacteria, can inactivate the macrolides. [Pg.412]

Directed evolution involves multiple rounds of random mutation and selection combined with gene shuffling to evolve enzymes towards desired properties (reviewed in Arnold and Moore, 1997 Kuchner and Arnold, 1997). The group of Arnold has succeeded in evolving a dimethylformamide (DMF)-sensitive esterase for the cleavage of the loracarbef-/>-nitrobenzyl ester into an esterase that remains active in 15% DW (Moore et al, 1997). Most of the mutations that had been found in the solvent-resistant mutants could not have been predicted using current computational methods. [Pg.205]

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... [Pg.71]


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See also in sourсe #XX -- [ Pg.211 ]




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