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神经毒素 β-N-甲基氨基-L-丙氨酸对石斑鱼受精和早期发育的抑制作用。

Inhibitory effects of neurotoxin β-N-methylamino-L-alanine on fertilization and early development of the sea urchin Lytechinus pictus.

机构信息

College of Environmental Science and Engineering, Ocean University of China, Qingdao 266100, China; Key Laboratory of Marine Environment and Ecology, Ocean University of China, Ministry of Education, Qingdao 266100, China.

Marine Biology Research Division, Scripps Institution of Oceanography, University of California San Diego, La Jolla, CA 92093-0202, USA.

出版信息

Aquat Toxicol. 2020 Apr;221:105425. doi: 10.1016/j.aquatox.2020.105425. Epub 2020 Jan 30.

DOI:10.1016/j.aquatox.2020.105425
PMID:32058875
Abstract

Neurotoxin β-N-methylamino-L-alanine (BMAA) has been widely detected in diverse aquatic organisms and hypothesized as an environmental risk to neurodegenerative diseases in humans. However, the knowledge of its toxicity to marine organisms requires attention. In the present study, embryos and sperm of the sea urchin, Lytechinus pictus, were used to assess the toxicity of BMAA. Effects of BMAA on fertilization and development of sea urchin embryos were measured, and its impacts on efflux transport of sea urchin blastula were also assayed. Results demonstrated that the fertilization and development of embryos were significantly inhibited by high concentrations of BMAA above 300 μg L. The EC values indicated by active swimming larvae and total larvae numbers at 96 HPF (hours post fertilization) were 165 μg L (1.4 μmol L) and 329 μg L (2.8 μmol L), respectively. Additionally, sperm exposed to BMAA for 10 min significantly reduced the fertilization ratio of sea urchin eggs. However, the ABC transport activity on the cytomembrane of sea urchin blastula was not inhibited by the presence of BMAA at 50 μg L, even up to 500 μg L. Abnormal division and developmental malformations occurred at different developmental stages for sea urchin embryos exposed to BMAA at 500 μg L. The inhibitory effects of BMAA on sea urchin embryos were reported at the first time in this study, for which the toxicological mechanisms will be explored in future studies.

摘要

神经毒素 β-N-甲基氨基-L-丙氨酸 (BMAA) 已广泛存在于各种水生生物中,并被假设为人类神经退行性疾病的环境风险因素。然而,其对海洋生物的毒性的认识仍需要关注。在本研究中,使用了石斑鱼(Lytechinus pictus)的胚胎和精子来评估 BMAA 的毒性。测量了 BMAA 对海胆胚胎受精和发育的影响,并检测了其对海胆囊胚外排转运的影响。结果表明,高浓度(高于 300μg/L)的 BMAA 显著抑制胚胎的受精和发育。在 96 HPF(受精后小时)时,通过活跃游动幼虫和总数幼虫数表示的 EC 值分别为 165μg/L(1.4μmol/L)和 329μg/L(2.8μmol/L)。此外,暴露于 BMAA 10 分钟的精子显著降低了海胆卵的受精率。然而,即使在 500μg/L 的浓度下,BMAA 也不会抑制海胆囊胚质膜上的 ABC 转运活性。在 500μg/L 的 BMAA 暴露下,海胆胚胎在不同发育阶段出现了异常分裂和发育畸形。本研究首次报道了 BMAA 对海胆胚胎的抑制作用,未来的研究将探讨其毒性作用机制。

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