Evidence for the ability of organotins to act as endocrine-disrupting chemicals (EDCs) has been
accumulating over the past couple of decades. One of the most consistently cited examples of environmental
endocrine disruption in wildlife is the occurrence of male sex characteristics on female neogastropods, termed
imposex, as a result of exposure to tributyltin (TBT). Extensive efforts have been made to elucidate the
mechanism by which TBT induces imposex. A hypothesis regarding the elevation of testosterone by TBT has
been widely touted as a result of the association between exposure to TBT and increased free testosterone titers in
imposexed females. The hypothesis specifically states that TBT elevates testosterone which then initiates some
unknown biochemical signaling pathway with the ultimate outcome being the development of imposex. Recently,
some organotins, including TBT, were shown to be high-affinity ligands of vertebrate retinoid X-receptors
(RXRs). This finding has resulted in the development and testing of the latest hypothesis for TBT-induced
imposex: TBT causes imposex by disrupting retinoid signaling, i.e., retinoic acid acting via the RXR. Studies
suggesting that RXR signaling may be important in the development of the reproductive tract in neogastropods
provide additional support for the involvement of retinoid signaling in the development of imposex. Future
research regarding the mechanism of TBT-induced imposex should focus on identifying pathways downstream of
RXR binding that are involved in reproductive tract development in neogastropods.
Keywords: Tributyltin - imposex - testosterone- acyl coenzyme A: testosterone acyltransferase - retinoid Xreceptor.
