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Additionally, these insects tend to be relatively large, long-lived, active, and frequently aggregate. [2] Indeed, longer-lived insects are more likely to be chemically defended than short lived ones, as longevity increases apparency. [9] Throughout the arthropod and insect realm, however, chemical defenses are quite unevenly distributed.
Plants maintain an ability to sense when they have an injured area and induce a defensive response. Within wounded tissues, endogenous molecules become released and become Damage Associated Molecular Patterns (DAMPs), inducing a defensive response. DAMPs are typically caused by insects that feed off the plant. [2]
Chemical defense is a strategy employed by many organisms to avoid consumption by producing toxic or repellent metabolites or chemical warnings which incite defensive behavioral changes. [ 1 ] [ 2 ] The production of defensive chemicals occurs in plants, fungi, and bacteria, as well as invertebrate and vertebrate animals.
Plants have evolved many defense mechanisms against insect herbivory in the 350 million years in which they have co-evolved.Such defenses can be broadly classified into two categories: (1) permanent, constitutive defenses, and (2) temporary, inducible defenses. [1]
Some chemical defenses once thought to be produced by the plant have since been shown to be synthesized by endophytic fungi. The chemical basis of insect resistance in endophyte-plant defense mutualisms has been most extensively studied in the perennial ryegrass and three major classes of secondary metabolites are found: indole diterpenes, ergot alkaloids and peramine.
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Chemical communication in insects is social signalling between insects of the same or different species, using chemicals. These chemicals may be volatile, to be detected at a distance by other insects' sense of smell, or non-volatile, to be detected on an insect's cuticle by other insects' sense of taste.
There are two types of pyrethroids: those with and without α-cyanogroup. The neurotoxicity of bifenthrin is based on the affinity to the voltage-gated sodium channels (in insects as well as mammals). The pyrethroids with an α-cyanogroup block the sodium-channel permanently, causing the membrane to be permanently hyperpolarized.