Figure 6.

Conjectural model of the role of CSP in activation of linoleic acid/omega6 fatty acid-diacylglycerol pathway upon xenobiotic insecticide or juvenile hormone exposure. (1) Some insect cells have the ability to synthesize linoleic acid (C18:2) de novo using fourteen-eighteen carbons-fatty acids (C14–C18) and specific desaturases. (2) C18:2 is fuel molecule for omega6 fatty acid pathways. Molecules such as arachidonyl-CoA ((Z5,Z8,Z11,Z14)-Icosatetraenoyl-CoA or C20:4) are products of a ∆5 desaturase reaction from eicosatrienoyl-CoA (C20:3) as a direct substrate. (3) Synthesis of these fatty acid metabolites leads to phosphatidic acid and therefore to the formation of diacylglycerol (DAG) through the biosynthetic pathway of glycerol-phosphatydilcholins. (4) DAG is a relay molecule in intracellular cascades activated by the binding of regulatory chemical ligand (labelled by a black triangle) to G-protein coupled receptor. This triggers the formation of inositol 1,4,5-triphosphate (IP3) and DAG by PLC (phospholipase C). In turn, IP3 releases the calcium ions (Ca⁺⁺) from intracellular stocks in the endoplasmic reticulum (ER). (5) DAG (with Ca⁺⁺) activates (+) protein kinase C (PKC), which in turn induces specific cellular responses by phosporylating a particular set of cellular proteins (ion channels, myosin, cytochrome P450, desaturase enzymes, etc.). Applying xenobiotic insecticide and/or juvenile hormone (JH) activates (+) the DAG pathway and thereby protein phosphorylation (red symbol P) via increased concentrations of C18 and C20 fatty acids on cell growth performance and/or immune response of various tissues, organs and organ systems. The green arrow means that the concentration of C18:2, C18:3 and DAG increases with increasing concentration of xenobiotic insecticides and/or JH. The central role for CSP in ∆12-fatty acid pathway associated with transport of C18:2 for multifunction, immunity, cell development, tissue growth and neuronal plasticity is shown in red.