Effects of α-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 α-mangostin on embryonic development and hepatogenesis in zebrafish. Result Exposure of embryos to 0.25–4 μM α-mangostin from 4–120 h post-fertilization (hpf) caused mortality of embryos with LC 50 1.48 ± 0.29 μM. The compound also caused deformities, including head malformation, pericardial oedema, absence of swim bladder, yolk oedema, and bent tail. Exposure of zebrafish embryos to α-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).