Quilliam M A
Institute for Marine Biosciences, National Research Council of Canada, Halifax, Nova Scotia, Canada.
J AOAC Int. 1999 May-Jun;82(3):773-81.
The 1997-1998 period brought many new developments to the phycotoxin field. There were several reviews on phycotoxins in general, on their toxicological evaluation, and on their analysis. The ecophysiology, biosynthesis, and metabolism of polyether toxins and paralytic shellfish poisoning (PSP) toxins were also reviewed. The proceedings of the Eighth International Conference on Harmful Algae (Vigo, Spain, June 25-29, 1997) have been published and provide an excellent source of information on phycotoxins and toxic plankton bloom research. In addition, the much anticipated proceedings of the IX International IUPAC Symposium on Mycotoxins and Phycotoxins (Rome, Italy, May 27-31, 1996) have been published. Further evidence was provided to support the theory that Prorocentrum lima is the source organism for diarrhetic shellfish poisoning (DSP) toxins in Nova Scotian shellfish. In another study, different Prorocentrum species and isolates were analyzed for DSP toxins. In addition to detecting some new compounds, such as a DTX1 isomer, it was found that toxins were produced by both axenic and nonaxenic batch cultures, indicating that bacteria are probably not involved in the biosynthesis. The source organism for the spirolides, a family of fast-acting toxins reported from Nova Scotia, Canada, was determined to be Alexandrium ostenfeldii, a species that is found worldwide. The biogenetic origin of yessotoxin was reported to be Protoceratium reticulatum, another widely occurring organism. A great deal of attention and research funding has been directed at the serious problems associated with Pfiesteria piscicida. Analysts are eagerly awaiting publication of toxin structures, which will then allow the development of analytical methods. An incident of the mass mortality of California sea lions was reported in the Monterey area in May 1998. Analyses of tissue and urine samples revealed the presence of domoic acid. High levels of domoic acid were also found in anchovies and sardines, a common food source of sea lions. This is reminiscent of an incident of mass bird mortality in 1992 in the same region. Toxicological studies of domoic acid continue with one investigation on the effect of pH on toxicity in the mouse assay and others examining toxic effects in rats and cynomolgus monkeys. A study on the uptake and depuration of domoic acid in the Dungeness crab was reported. On October 20, 1997, EU (European Union) directive CE97/61 established a regulatory limit of 20 ppm for domoic acid in European shellfish, the same level as in North America. A detailed study on the oral toxicity of DSP toxins in mice was reported. Recent work by several researchers has revealed the genotoxic potential of okadaic acid and other DSP toxins. Previous work had clearly demonstrated the tumor-promoting potential of DSP toxins, but this recent evidence, which shows mutations in the progeny of okadaic acid-treated cells and the formation of DNA-adducts, increases concerns over the hazards associated with DSP-contaminated shellfish. The toxicology of yessotoxin was evaluated by Ogino et al. The toxin showed weak cytotoxicity, but was not orally lethal to mice at 10 mg/kg, and did not cause intestinal fluid accumulation, inhibition of protein phosphatase 2A (PP2A), or hemolytic effects. Similarly, Tubaro et al. saw no evidence for diarrheogenicity of homoyessotoxin isolated from mussels and from the proposed planktonic producer, Lingulodinium polyedrum. All this provides further evidence that yessotoxin should not be classed as a DSP toxin. A number of new toxins have been detected and identified. Two analogues of yessotoxin, homoyessotoxin, and 45-hydroxyhomoyessotoxin were isolated from mussels of the Adriatic Sea and identified by Satake et al. A recent DSP event in Ireland associated with cultured mussels led to the identification of azaspiracid, a unique marine toxin with spiro ring assemblies. (ABSTRACT TRUNCATED)
1997年至1998年期间,藻毒素领域有许多新进展。发表了几篇关于藻毒素的综述,涵盖了藻毒素的总体情况、毒理学评价及其分析方法。还对聚醚毒素和麻痹性贝类毒素(PSP)的生态生理学、生物合成及代谢进行了综述。第八届国际有害藻类会议(1997年6月25日至29日,西班牙维戈)的会议记录已出版,是藻毒素和有毒浮游生物大量繁殖研究的重要信息来源。此外,备受期待的第九届国际纯粹与应用化学联合会(IUPAC)霉菌毒素与藻毒素研讨会(1996年5月27日至31日,意大利罗马)的会议记录也已出版。有进一步证据支持利马原甲藻是新斯科舍贝类中腹泻性贝类毒素(DSP)来源生物的理论。在另一项研究中,对不同的原甲藻物种和分离株进行了DSP毒素分析。除检测到一些新化合物,如DTX1异构体,还发现无菌和非无菌分批培养物均能产生毒素,这表明细菌可能不参与生物合成。加拿大新斯科舍报道的一类速效毒素——螺旋环肽的来源生物被确定为在全球广泛分布的奥氏亚历山大藻。报道称,虾夷毒素的生物起源是网状原角藻,这也是一种广泛分布的生物。与杀鱼费氏藻相关的严重问题受到了大量关注并获得了研究资金。分析人员急切期待毒素结构的发表,以便开发分析方法。1998年5月,蒙特雷地区报道了加利福尼亚海狮大量死亡事件。对组织和尿液样本的分析显示存在软骨藻酸。在凤尾鱼和沙丁鱼(海狮常见食物来源)中也发现了高含量的软骨藻酸。这让人想起1992年同一地区发生的鸟类大量死亡事件。继续开展软骨藻酸的毒理学研究,其中一项研究是关于pH对小鼠毒性测定的影响,其他研究则是检测其对大鼠和食蟹猴的毒性作用。报道了一项关于珍宝蟹对软骨藻酸的摄取和清除的研究。1997年10月20日,欧盟指令CE97/61规定欧洲贝类中软骨藻酸的监管限量为20 ppm,与北美相同。报道了一项关于DSP毒素对小鼠口服毒性的详细研究。几位研究人员最近的工作揭示了冈田酸和其他DSP毒素的遗传毒性潜力。此前的研究已明确证明DSP毒素具有促肿瘤潜力,但最近的证据显示,经冈田酸处理的细胞后代发生突变并形成DNA加合物,这增加了人们对受DSP污染贝类相关危害的担忧。荻野等人对虾夷毒素的毒理学进行了评估。该毒素显示出较弱的细胞毒性,但在10 mg/kg剂量下对小鼠口服无致死性,也未引起肠液积聚、蛋白磷酸酶2A(PP2A)抑制或溶血效应。同样,图巴罗等人未发现从贻贝及假定的浮游生物生产者多甲藻中分离出的高虾夷毒素具有致腹泻性的证据。所有这些都进一步证明虾夷毒素不应归类为DSP毒素。已检测并鉴定出多种新毒素。萨塔克等人从亚得里亚海贻贝中分离出虾夷毒素的两种类似物、高虾夷毒素和45 - 羟基高虾夷毒素并进行了鉴定。爱尔兰最近发生的一起与养殖贻贝相关的DSP事件导致了azaspiracid(一种具有螺环结构的独特海洋毒素)的鉴定。