Effects of alpha-mangostin on embryonic development and liver development in zebrafish

Background Alpha-mangostin has potential as a chemopreventive agent but there is little information on its toxicological profile and developmental toxicity. Objective We evaluated the effects of alpha-mangostin on embryonic development and hepatogenesis in zebrafish. Result Exposure of embryos to 0.25-4 mu M alpha-mangostin from 4-120 h post-fertilization (hpf) caused mortality of embryos with LC50 1.48 +/- 0.29 mu M. The compound also caused deformities, including head malformation, pericardial oedema, absence of swim bladder, yolk oedema, and bent tail. Exposure of zebrafish embryos to alpha-mangostin during early hepatogenesis (16-72 hpf) decreased the transcript expression levels of liver fatty acid-binding protein 10a (Fabp10a), but increased gene markers of inflammation, oxidative stress, and apoptosis. In Fabp10a:DsRed transgenic zebrafish, the intensity and the area of fluorescence in the liver of the treated group were decreased (non-significantly) relative to controls. Conclusion These effects were more marked during early hepatogenesis (16-72 hpf) than during post-hepatogenesis (72-120 hpf).