| Autor: |
Pimtong, Wittaya, Kitipaspallop, Wannakarn, Chun, Hang-Suk, Kim, Woo-Keun |
| Zdroj: |
Molecular & Cellular Toxicology; Nov2020, Vol. 16 Issue 4, p469-476, 8p |
| Abstrakt: |
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 LC50 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). [ABSTRACT FROM AUTHOR] |
| Databáze: |
Complementary Index |
| Externí odkaz: |
|
Full text from SpringerLink