National Pathogen Collection Center for Aquatic Animals, Shanghai Ocean University, Shanghai 201306, China; Key Laboratory of Exploration and Utilization of Aquatic Genetic Resources, Ministry of Education, Shanghai Ocean University, Shanghai Ocean University, Shanghai 201306, China.
National Pathogen Collection Center for Aquatic Animals, Shanghai Ocean University, Shanghai 201306, China.
Aquat Toxicol. 2024 Nov;276:107090. doi: 10.1016/j.aquatox.2024.107090. Epub 2024 Sep 10.
This study evaluates the impact of environmentally relevant, low-concentration deltamethrin exposure to Eriocheir sinensis ovaries. Our findings revealed that even at a concentration of 0.05 µg/L, deltamethrin exposure can induce significant ovarian toxicity through a 5-day exposure, with gradual amplification detected with time, demonstrating the toxicity amplification effect. Hematoxylin and Eosin staining revealed that low-concentration deltamethrin exposure produces pathological damage consistent with acute toxicity-yolk granules were dissolved and oocyte membranes were ruptured. High-throughput RNA-sequencing data indicated that the acute and low-concentration exposure groups involved completely different pathways and molecular functions, suggesting distinct mechanisms for their toxic effects. Following the identification of phospholipase D (PLD) as a potential core factor regulating the toxicity amplification effect of low concentration deltamethrin, we delved into subsequent mechanism studies using quantitative real-time PCR, immunofluorescence and enzyme-linked immunosorbent assay. Through the GnRH signaling pathway, increased PLD indirectly stimulates augmented estradiol secretion, subsequently inducing apoptosis by upregulating Cathepsin D, which can activate the key executioners of apoptosis-caspases (CASP3 and CASP7). In conclusion, low-concentration deltamethrin exposures can induce significant ovarian damage through apoptosis mediated by the upregulation of PLD in the ovaries of Eriocheir sinensis at environmentally relevant concentrations, which lays the preliminary theoretical groundwork for further elucidating the mechanism of toxicity amplification effect of pesticide exposure at low concentrations.
本研究评估了环境相关浓度的低浓度溴氰菊酯对中华绒螯蟹卵巢的影响。我们的研究结果表明，即使在 0.05μg/L 的浓度下，溴氰菊酯暴露也会通过 5 天的暴露引起显著的卵巢毒性，随着时间的推移逐渐放大，表现出毒性放大效应。苏木精-伊红染色显示，低浓度溴氰菊酯暴露会产生与急性毒性一致的病理性损伤——卵黄颗粒溶解，卵母细胞膜破裂。高通量 RNA 测序数据表明，急性和低浓度暴露组涉及完全不同的途径和分子功能，提示其毒性作用具有不同的机制。在确定磷脂酶 D（PLD）作为调节低浓度溴氰菊酯毒性放大效应的潜在核心因素后，我们使用定量实时 PCR、免疫荧光和酶联免疫吸附测定法进一步研究了后续的机制。通过 GnRH 信号通路，增加的 PLD 间接刺激雌激素的分泌增加，随后通过上调组织蛋白酶 D 诱导细胞凋亡，组织蛋白酶 D 可以激活凋亡的关键执行者——胱天蛋白酶（CASP3 和 CASP7）。总之，在环境相关浓度下，低浓度溴氰菊酯暴露会通过中华绒螯蟹卵巢中 PLD 的上调介导凋亡，导致显著的卵巢损伤，这为进一步阐明低浓度农药暴露毒性放大效应的机制奠定了初步的理论基础。
