Kumar K Prem, Kumar Sreeletha Prem, Nair G Achuthan
ENBIOMON, 1205 Seaton et, Montgomery, Alabama 36117, USA.
J Environ Biol. 2009 May;30(3):319-25.
Risk assessment of the amnesic shellfish poison, domoic acid, a potent neurotoxin, is evaluated based on its current knowledge and its harmful effects, and is presented under four headings, viz., (1) hazard identification, (2) dose response assessment, (3) exposure assessment and (4) risk characterization. Domoic acid binds the glutamate receptor site of the central nervous system (CNS) of humans and causes depolarization of neurons and an increase in cellularcalcium. In nature, domoic acid is produced by the algae, Pseudonitzschia spp. and they enter into the body of shellfish through their consumption. This toxin is reported to cause gastroenteritis, renal insufficiency confusion and memory loss in humans, since it affects the hippocampus of the brain. In rats, intraperitonial and oral administration of domoic acid result in scratching, tremor and convulsions, and in monkeys, the toxic symptoms like mastication, salivation, projectile vomiting, weakness, teeth grinding and lethargy are apparent. The no-observed-adverse-effect-level (NOAEL) in animals reveals that pure toxin is more effective than those isolated from shellfish. Based on LD50 values, it is found that intraperitonial administration of this toxin in animals is 31 fold more effective than oral administration. Low levels of domoic acid (0.20-0.75 ppm) show no toxic symptoms in non-human primates, but clinical effects are apparent in them and in humans, at a concentration of 1.0 ppm. The tolerable daily intake (TDI) of domoic acid for humans is calculated as 0.075 ppm, whereas for razor clams and crabs, the TDI are 19.4 and 31.5 ppm respectively. The hazard quotient (HQ) is found to be 2. Being an irreversible neurotoxin, domoic acid has severe public health implications. Death occurs in those above 68 years old. In order to ensure adequate protection to public health, the concentration of domoic acid in shellfish and shellfish parts at point of sale shall not exceed the current permissible limit of 20 microg g(-1) tissue. While processing shellfish, it maybe advisable to pay attention to factors such as environmental conditions, inter-organ variability in concentrations of domoic acid and cross contaminations.
失忆性贝类毒素——软骨藻酸是一种强效神经毒素，基于其现有认知和有害影响对其进行风险评估，并在以下四个标题下进行阐述，即：(1) 危害识别，(2) 剂量反应评估，(3) 暴露评估和 (4) 风险特征描述。软骨藻酸与人类中枢神经系统 (CNS) 的谷氨酸受体位点结合，导致神经元去极化并使细胞内钙增加。在自然界中，软骨藻酸由拟菱形藻属藻类产生，它们通过贝类摄食进入贝类体内。据报道，这种毒素会导致人类肠胃炎、肾功能不全、意识混乱和失忆，因为它会影响大脑的海马体。在大鼠中，腹腔注射和口服软骨藻酸会导致抓挠、震颤和抽搐，在猴子中，会出现咀嚼、流涎、喷射性呕吐、虚弱、磨牙和嗜睡等中毒症状。动物的未观察到有害作用水平 (NOAEL) 表明，纯毒素比从贝类中分离出的毒素更具效力。根据半数致死剂量 (LD50) 值发现，在动物中腹腔注射这种毒素的效力比口服高 31 倍。低水平的软骨藻酸 (0.20 - 0.75 ppm) 在非人类灵长类动物中未显示出中毒症状，但在浓度为 1.0 ppm 时，它们和人类会出现明显的临床效应。人类对软骨藻酸的每日耐受摄入量 (TDI) 计算为 0.075 ppm，而对于蛏子和螃蟹，TDI 分别为 19.4 和 31.5 ppm。危害商数 (HQ) 为 2。作为一种不可逆的神经毒素，软骨藻酸对公众健康有严重影响。68 岁以上的人会死亡。为确保对公众健康的充分保护，贝类及其可食用部分在销售点的软骨藻酸浓度不得超过当前允许的 20 μg g(-1) 组织的限量。在加工贝类时，可能建议关注环境条件、软骨藻酸浓度的器官间变异性和交叉污染等因素。
