A possible speculation on the involvement of ROS and lysosomes mediated mitochondrial pathway in apoptosis of rotifer Brachionus plicatilis with BDE-47 exposure
A possible speculation on the involvement of ROS and lysosomes mediated mitochondrial pathway in apoptosis of rotifer Brachionus plicatilis with BDE-47 exposure
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ROS 和溶酶体介导的线粒体途径参与 BDE-47 暴露的褶皱臂尾轮虫凋亡的可能推测
DOI：
10.1016/j.scitotenv.2021.147315
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发表时间：
2021-05-20
影响因子：
9.8
通讯作者：
Wang, You
中科院分区：
文献类型：
--
作者：
Wang, Boyuan;Guo, Ying;Wang, You
本文研究了海洋生态系统中分布最广、最具生物毒性的溴化阻燃剂（PBDEs）之一的2,2′，4,4′-四溴联苯醚（BDE-47）对海洋轮虫（Brachionus plicatilis）的毒性和细胞凋亡，并从线粒体途径的角度创新性地探讨了其可能的作用机制。BDE-47连续暴露（0.08、0、8和8 mg/L）可导致线粒体膜电位（MMP）下降，荧光强度增强，胃和卵巢的MMP下降明显，提示细胞发生凋亡。透射电镜观察显示卵巢线粒体超微结构明显受损。由此推测并证实了线粒体- ros过量产生-细胞凋亡的途径。我们首先发现，BDE-47诱导促凋亡蛋白Bax和抗凋亡蛋白Bcl-2 （Bax/Bcl-2）比值升高，线粒体通路关键成分caspase-9和-3活性明显呈浓度依赖性，同时ROS生成发生改变。预处理ROS抑制剂不仅能显著降低ROS升高，还能在一定程度上降低Bax/Bcl-2比值，且ROS与Bax/Bcl-2比值呈正相关。有趣的是，在0.08和0.8 mg/L组中，首先观察到有丝分裂发生在被破坏的白滑桃超微结构中，并且自噬体的初步证据可以推测其参与响应BDE-47胁迫。综上所述，我们提出BDE-47破坏线粒体，导致ROS过量产生，随后启动线粒体途径。推测认为，细胞凋亡和线粒体自噬都参与了白僵菌应对BDE-47暴露的过程。(C) 2021 Elsevier B.V.版权所有
The toxicity and apoptosis induced by 2,2 ',4,4 '-tetrabromodiphenyl ether (BDE-47), one of the most widespread and bio-toxic brominated flame retardants (PBDEs) in marine ecosystem, were investigated and the possibly responsible mechanism was innovatively discussed from the perspective of mitochondrial pathway in marine rotifer Brachionus plicatilis. A series of BDE-47 exposure (0.08, 0,8 and 8 mg/L) led to the decrease of mitochondrial membrane potential (MMP) based on the strengthened fluorescence intensity, especially on stomach and ovary, which indicated the occurrence apoptosis. Further transmission electron microscopy (TEM) observation showed distinct ultrastructure impairment on mitochondria in the ovary. A pathway of mitochondria-ROS overproduction-apoptosis was thus speculated and proved. We first found that BDE-47 induced the increment of the ratio of pro-apoptosis protein Bax and anti-apoptosis protein Bcl-2 (Bax/Bcl-2), as well as the activities of key components caspase-9 and -3 in mitochondrial pathway in a clear concentration-dependent manner, accompanied by the simultaneous alteration of ROS production. The pretreatment of ROS inhibitor not only significantly attenuated ROS elevation but also decreased Bax/Bcl-2 ratio to some extent, and a strong positive correlation was found between ROS and Bax/Bcl-2 ratio. Interestingly, mitophagy was firstly observed in the damaged ultrastructure of B. plicatilis in 0.08 and 0.8 mg/L group, and the preliminary evidence of autophagosomes enabled the speculation of its involvement responding to BDE-47 stress. Taken together, we proposed that BDE-47 damaged the mitochondria that led to ROS overproduction, followed by the initiation of mitochondrial pathway. Speculatively, both apoptosis and mitophagy were assumed to involve in B. plicatilis coping with BDE-47 exposure. (C) 2021 Elsevier B.V. All rights reserved.