Department of Lifescience and Biotechnology, College of Chemistry, Chemical Engineering and Life Sciences, Wuhan University of Technology, Wuhan 430070, PR China.
Department of Lifescience and Biotechnology, College of Chemistry, Chemical Engineering and Life Sciences, Wuhan University of Technology, Wuhan 430070, PR China.
Aquat Toxicol. 2016 Jul;176:106-15. doi: 10.1016/j.aquatox.2016.04.014. Epub 2016 Apr 21.
Aphantoxins from Aphanizomenon flos-aquae are frequently identified in eutrophic waterbodies worldwide. These toxins severely endanger environmental safety and human health due to the production of paralytic shellfish poisons (PSPs). Although the molecular mechanisms of aphantoxin neurotoxicity have been studied, many questions remain to be resolved such as in vivo alterations in branchial histology and neurotransmitter inactivation induced by these neurotoxins. Aphantoxins extracted from a naturally isolated strain of A. flos-aquae DC-1 were determined by high performance liquid chromatography. The basic components of the isolated aphantoxins identified were gonyautoxin 1 (GTX1), gonyautoxin 5 (GTX5), and neosaxitoxin (neoSTX), which comprised 34.04, 21.28, and 12.77% of the total, respectively. Zebrafish (Danio rerio) was administrated 5.3 or 7.61mg STX equivalents (eq)/kg (low and high doses, respectively) of the A. flos-aquae DC-1 aphantoxins by intraperitoneal injection. Histological alterations and changes in neurotransmitter inactivation in the gills of zebrafish were investigated for 24h following exposure. Aphantoxin exposure significantly increased the activities of gill alanine aminotransferase (ALT) and aspartate aminotransferase (AST) and resulted in histological alterations in the gills during the first 12h of exposure, indicating the induction of functional and structural damage. Gill acetylcholinesterase (AChE) and monoamine oxidase (MAO) activities were inhibited significantly, suggesting an alteration of neurotransmitter inactivation in zebrafish gills. The observed alterations in gill structure and function followed a time- and dose-dependent pattern. The results demonstrate that aphantoxins or PSPs lead to structural damage and altered function in the gills of zebrafish, including changes in histological structure and increases in the activities of AST and ALT. The inhibition of the activities of AChE and MAO suggest that aphantoxins or PSPs could induce respiratory toxicity in the zebrafish gill. Furthermore, these parameters may be used as bioindicators for investigating aphantoxin exposure and cyanobacterial blooms in nature.
从水华鱼腥藻中分离出的拟鱼腥藻毒素经常在全世界富营养化的水体中被发现。由于产生麻痹性贝类毒素（PSP），这些毒素严重危害环境安全和人类健康。尽管拟鱼腥藻毒素的神经毒性的分子机制已经被研究，但仍有许多问题有待解决，例如这些神经毒素在体内引起的鳃组织学改变和神经递质失活。通过高效液相色谱法测定了从天然分离的鱼腥藻水华 DC-1 菌株中提取的拟鱼腥藻毒素。分离出的拟鱼腥藻毒素的基本成分分别为 GTX1、GTX5 和 neoSTX，占总毒素的 34.04%、21.28%和 12.77%。通过腹腔注射，将斑马鱼（Danio rerio）用 5.3 或 7.61mgSTX 当量（eq）/kg（低剂量和高剂量）的鱼腥藻水华 DC-1 拟鱼腥藻毒素处理。暴露后 24 小时，研究了斑马鱼鳃中的组织学改变和神经递质失活的变化。拟鱼腥藻毒素暴露显著增加了鳃丙氨酸氨基转移酶（ALT）和天冬氨酸氨基转移酶（AST）的活性，并在暴露的前 12 小时导致鳃的组织学改变，表明功能和结构损伤的诱导。鳃乙酰胆碱酯酶（AChE）和单胺氧化酶（MAO）的活性显著抑制，表明斑马鱼鳃中的神经递质失活发生改变。鳃结构和功能的改变呈现出时间和剂量依赖性模式。结果表明，拟鱼腥藻毒素或 PSP 导致斑马鱼鳃的结构和功能损伤，包括组织学结构的改变以及 AST 和 ALT 活性的增加。AChE 和 MAO 活性的抑制表明，拟鱼腥藻毒素或 PSP 可能在斑马鱼鳃中引起呼吸毒性。此外，这些参数可作为研究拟鱼腥藻暴露和天然水华的生物标志物。
