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Abstract
The esterase-based insecticide resistance mechanisms characterised to date predominantly
involve elevation of activity through gene amplification allowing increased levels
of insecticide sequestration, or point mutations within the esterase structural genes
which change their substrate specificity. The amplified esterases are subject to various
types of gene regulation in different insect species. In contrast, elevation of glutathione
S-transferase activity involves upregulation of multiple enzymes belonging to one
or more glutathione S-transferase classes or more rarely upregulation of a single
enzyme. There is no evidence of insecticide resistance associated with gene amplification
in this enzyme class. The biochemical and molecular basis of these two metabolically-based
insecticide resistance mechanisms is reviewed.