Paralytic shellfish poisoning in southern China
Paralytic shellfish poisoning in southern China
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DOI：
10.1016/0041-0101(95)00158-1
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发表时间：
1996-05-01
期刊：
影响因子：
2.8
通讯作者：
Lin, YT
中科院分区：
文献类型：
--
作者：
Anderson, DM;Kulis, DM;Lin, YT
近30年来，中国南部沿海迅速扩张的海水养殖和商业区经历了零星的麻痹性贝类中毒暴发，但人们几乎不知道这种毒性或致病微生物的性质。这项研究首次将大亚湾麻风性贝毒暴发所涉及的贝类的高效液相色谱毒素组成谱与从该水域建立的塔玛亚历山大藻培养物进行了直接比较。被分析的三种培养物产生了不同寻常的高比例低效性N-硫代氨基甲酰毒素C1和C2(几乎占总数的90%)，而只有微量的其他萨克托毒素衍生物。因此，用温和的酸提取总毒性很低，范围在7.2至12.7fmolcell(-1)之间，或0.7-0.9pg的石杉毒素当量。单元格(-1)。用标准的AOAC萃取法进行酸解后，培养物中的主要毒素是弓形虫毒素2和3以及脱氨甲酰弓形虫毒素2和3。总效价提高了四倍，达到2.6-3.4pg的岩藻毒素当量。细胞(-1)在酸解后。因此，这些培养物处于塔玛弧菌复合体成员所记录的毒性范围的低端。在1990年和1991年的麻风性贝类中毒事件中，从大亚湾采集的两个扇贝和一个贻贝样本也按照AOAC提取程序进行了分析。三个贝类样本的毒素谱相似，因为每个样本中都存在相同的一套毒素，但这些毒素的相对比例有所不同。主要毒素为2号和3号毒素，以及1-C4毒素。扇贝和贻贝的总毒性分别为336和654微克/100g肉，贻贝为723微克/100g。毒素C3，4在贝类中的含量高达22%，但在培养物中检测不到C3，4毒素，即使使用温和的酸进行提取。尽管培养物的性质与贝类毒素特征相似，但C3，4的存在表明，另一种亚历山大藻或另一种可能产生麻痹性贝类毒素的物种是导致1990年和1991年大亚湾麻痹性贝类中毒爆发的原因。由于所分析的培养物具有较低的内在毒性，因此塔玛拉索杆菌在中国南岸的分布可能比过去麻痹性贝类中毒爆发的零星模式所暗示的更广泛。细胞密度高的水华需要产生足够的毒素才有危险。由于持续和日益严重的污染，中国水域藻类水华的数量惊人地增加，这可能会使这些低毒种群在未来更成问题。版权所有(C)1996爱思唯尔科学有限公司
The rapidly expanding mariculture and commercial region along the southern coast of China has experienced sporadic outbreaks of paralytic shellfish poisoning for nearly 30 years, yet virtually nothing is known of the nature of that toxicity or of the causative organisms. This study presents the first direct comparisons of the high performance liquid chromatography toxin composition profiles of shellfish implicated in paralytic shellfish poisoning outbreaks in Daya Bay with Alexandrium tamarense cultures established from those waters. The three cultures that were analyzed produced an unusually high proportion of the low potency N-sulfocarbamoyl toxins C1 and C2 (nearly 90% of the total), and only trace quantities of the other saxitoxin derivatives. Total toxicity was thus very low with mild acid extraction, ranging between 7.2 and 12.7 fmole cell(-1), or 0.7-0.9 pg saxitoxin equiv. cell(-1). Following acid hydrolysis using the standard AOAC extraction method, the dominant toxins in the cultures were gonyautoxins 2 and 3 and decarbamoyl gonyautoxins 2 and 3. Total potency increased fourfold to 2.6-3.4 pg saxitoxin equiv. cell(-1) following acid hydrolysis. These cultures are thus at the low end of the range of toxicities recorded for members of the A. tamarense species complex. Two scallop samples and one mussel sample collected from Daya Bay during paralytic shellfish poisoning episodes in 1990 and 1991 were also analyzed following the AOAC extraction procedure. The toxin profiles were similar for the three shellfish samples, in that the same suite of toxins were present in each, but the relative proportion of those toxins varied. The dominant toxins were gonyautoxins 2 and 3 and toxins C1-C4. Total toxicity was 336 and 654 mu g saxitoxin per 100 g meat for the scallop samples, and 723 for the mussels. Toxins C3,4 were present in the shellfish at up to 22 mole%, but were not detected in cultures, even when mild acid was used for extraction. Despite the otherwise similar nature of the culture versus the shellfish toxin signatures, the presence of C3,4 indicates that another strain or species of Alexandrium, or possibly a paralytic shellfish poisoning-producing species of another genus was responsible for the 1990 and 1991 paralytic shellfish poisoning outbreaks in Daya Bay. Since the cultures analyzed were of low intrinsic toxicity, A. tamarense may be more widespread along the south coast of China than is suggested by the sporadic pattern of past paralytic shellfish poisoning outbreaks. Blooms with high cell densities are required to generate sufficient toxin to be dangerous. The alarming increase in algal blooms in Chinese waters due to persistent and growing pollution may make these low toxicity populations more problematic in the future. Copyright (C) 1996 Elsevier Science Ltd