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Effects of methoprene, its metabolites, and breakdown products on retinoid‐activated pathways in transfected cell lines

Mthoprene (isopropyl (2E, 4E)‐11‐methoxy‐3,7,11‐trimethyl‐2,4‐dodecadienoate) is an insect juvenile hormone agonist that blocks metamorphosis in some insects. Recent evidence suggests that a metabolite, methoprene acid, activates vertebrate retinoid X receptors (RXRs), and may interfere with retinoic acid‐regulated developmental processes. Methoprene, methoxy‐methoprene acid, and two major breakdown products were tested for their ability to interfere with retinoid‐regulated pathways when using transfected cells. The CV‐1 cells were transiently transfected with genes encoding RXRs and response elements attached to luciferase reporters, and retinoic acid‐sensitive F9 cells were stably transfected with retinoic acid receptor (RAR)/RXR response elements attached a lacZ reporter (Sil‐REM/β‐gal‐NEO). Experiments confirmed that methoxy‐methoprene acid acted as a ligand for RXRs and was capable of activating transcription through RAR/RXR response elements. However, neither methoprene nor the breakdown products, 7‐methoxycitronellal and 7‐methoxycitronellic acid, activated transcription in transfected CV‐1 or F9 cells. Methoprene and methoxy‐methoprene acid may interfere with the conversion of all‐trans‐retinol and all‐trans‐retinaldehyde to all‐trans‐retinoic acid in the F9‐derived cell line. Methoprene was as effective as the retinol dehydrogenase inhibitor citral in blocking the retinol‐induced transcription of RAR/RXR‐regulated reporter genes, whereas methoxy‐methoprene acid blocked transcription stimulated by retinaldehyde.