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).

中文翻译：

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α-芒果素对斑马鱼胚胎发育和肝脏发育的影响

背景

Alman-Mangostin具有作为化学预防剂的潜力，但有关其毒理学特征和发育毒性的信息很少。

目的

我们评估了α-芒果对斑马鱼胚胎发育和肝发生的影响。

结果

受精后4–120 h（hpf），将胚胎暴露于0.25–4μMα-Mangostin导致LC ₅₀ 1.48± 0.29μM的胚胎死亡。该化合物还引起畸形，包括头部畸形，心包水肿，无游泳膀胱，卵黄水肿和弯曲的尾巴。斑马鱼胚胎在早期肝发生期间（16-72 hpf）暴露于α-Mangostin降低了肝脏脂肪酸结合蛋白10a（Fabp10a）的转录表达水平，但增加了炎症，氧化应激和凋亡的基因标记。在Fabp10a：DsRed转基因斑马鱼中，与对照组相比，治疗组肝脏的荧光强度和荧光面积均降低（无明显降低）。

结论

这些作用在早期肝发生期间（16–72 hpf）比在肝发生后阶段（72–120 hpf）更明显。