English (United Kingdom)

https://curated-unify.zendy.io/wp-json/zendy-region/v1/featured_content/oa?rat=en

https://curated-unify.zendy.io/wp-json/zendy-region/v1/highlighted_journal/

Global: Zendy Plus annual

Presents the access of premium content as premium feature

Premium Content

Presents the keyphrase highlighting as premium feature

Keyphrase Highlighting

Presents the summarisation as premium feature

Summarisation

Insights

Presents the pdf analysis as premium feature

PDF Analysis

Presents the zaia usage as premium feature

ZAIA

Global: Zendy Plus monthly

Global: Zendy Tools annual

Global: Zendy Tools monthly

Global: Zendy Free Plan

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).

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