Microcystin-LR promotes zebrafish (Danio rerio) oocyte (invivo) maturation by activating ERK1/2-MPF signaling pathways, and cAMP is involved in this process
Microcystin-LR promotes zebrafish (Danio rerio) oocyte (invivo) maturation by activating ERK1/2-MPF signaling pathways, and cAMP is involved in this process
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微囊藻毒素-LR 通过激活 ERK1/2-MPF 信号通路促进斑马鱼 (Danio rerio) 卵母细胞（体内）成熟，cAMP 参与此过程
DOI：
10.1016/j.envpol.2019.113843
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发表时间：
2020
影响因子：
8.9
通讯作者：
Xuezhen Zhang
中科院分区：
文献类型：
--
作者：
Chunhua Zhan;Feng Zhang;Wanjing Liu;Xuezhen Zhang
蓝藻水华及其次级代谢产物微囊藻毒素（Microcystins，MCs）不仅对水生生物具有毒性，而且对人类也有一定的危害。MCs通过影响卵母细胞的发育对雌性鱼类产生生殖毒性。然而，MC-LR干扰卵母细胞发育的机制在很大程度上仍然未知。本研究采用MC-LR（0、1、5、20 μg/L）染毒成年雌性斑马鱼30 d。暴露于MC-LR 30 d后，收集处理的雌性和健康雄性的受精卵，并在不含MC-LR的水中培养。组织形态学观察显示MC-LR暴露后卵巢出现病理损伤，其主要特征是细胞间隙扩大，卵泡细胞与卵母细胞分离，实质组织空泡化。20 μg/L MC-LR处理后，斑马鱼卵母细胞萌发囊泡破裂（GVBD）率显著增加，环磷酸腺苷（cAMP）和卵黄蛋白原（VTG）含量显著降低。此外，5和20 μ g/L MC-LR组斑马鱼卵巢细胞外信号调节激酶（ERK）磷酸化水平升高，20 μ g/L MC-LR组cyclinB磷酸化水平也显著上调。然而，MC-LR暴露在所有治疗中没有引起cAMP依赖性蛋白激酶（PKA）蛋白和cdc 2磷酸化水平的任何变化。MC-LR各剂量组均使卵数减少，受精卵提前孵化，子代畸形率增加。综上所述，本研究表明MC-LR通过激活ERK 1/2和MPF信号通路促进卵母细胞成熟，cAMP参与了这一过程。
Cyanobacterial blooms and their secondary metabolites, microcystins (MCs), are not only toxic to aquatic organisms, but also to humans. MCs exert reproductive toxicity in female fish by affecting the oocyte development. However, the mechanism behind MC-LR interference in oocyte development remains largely unknown. In our study, adult female zebrafish were exposed to MC-LR (0, 1, 5, 20 μg/L) for 30 d. After exposure to MC-LR for 30 d, fertilized eggs from the treated females and healthy males were collected and cultured in water without MC-LR. Histomorphological observations showed pathological damage in the ovary after MC-LR exposure, which was mainly characterized by enlarged intercellular spaces, detachment of follicular cells from oocytes, and vacuolation of parenchymal tissues. The 20 μg/L MC-LR treatment caused a remarkable increase in the rate of the zebrafish oocytes germinal vesicle breakdown (GVBD) and a significant decrease in the levels of cyclic adenosine monophosphate (cAMP) and vitellogenin (VTG). In addition, the phosphorylation levels of the extracellular signal-regulated kinases (ERK) were elevated in ovaries from zebrafish exposed to 5 and 20 μg/L MC-LR, and cyclinB phosphorylation levels were also upregulated notably in the 20 μg/L MC-LR group. However, MC-LR exposure did not cause any change in the levels of cAMP-dependent protein kinase (PKA) protein and cdc2 phosphorylation in all the treatments. All the doses of MC-LR reduced the number of eggs, prematurely hatched the fertilized eggs and increased the abnormal rate of offspring generation. In summary, the present study demonstrates that MC-LR promotes oocyte maturation by activating the ERK1/2 and MPF signaling pathways, and cAMP is involved in this process.