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作 者:李瑾祯 董晨帆 吴海燕[2] 邴晓菲 冯志华 谭志军[2,3] LI Jinzhen;DONG Chenfan;WU Haiyan;BING Xiaofei;FENG Zhihua;TAN Zhijun(Provincial Key Laboratory of Marine Biological Resources and Environment,Jiangsu Ocean University,Lianyungang 222000,China;Yellow Sea Fisheries Research Institute,Chinese Academy of Fishery Sciences,National Key Laboratory of Testing and Evaluation for Aquatic Product Safety and Quality,Ministry of Agriculture and Rural Affairs,Qingdao 266071,China;Pilot National Laboratory for Marine Science and Technology(Qingdao),Qingdao 266071,China)
机构地区:[1]江苏省海洋生物资源与环境重点实验室江苏海洋大学,江苏连云港222000 [2]中国水产科学研究院黄海水产研究所农业农村部水产品质量安全检测与评价重点实验室,山东青岛266071 [3]青岛海洋科学与技术试点国家实验室,山东青岛266071
出 处:《渔业科学进展》2023年第6期166-176,共11页Progress in Fishery Sciences
基 金:国家重点研发计划(2017YFC1600701);国家自然科学基金面上项目(41806138;31772075;32072329)共同资助。
摘 要:本研究将栉孔扇贝(Chlamys farreri)暴露于塔玛亚历山大藻(Alexandrium tamarense),通过测定内脏团中毒素的蓄积含量、氧化应激酶活性及其基因转录调控变化,探究栉孔扇贝暴露于麻痹性贝类毒素(Paralytic shellfish toxin,PSTs)的初期应激响应机制。结果显示,PSTs在内脏团中迅速蓄积,实验第6天时毒素含量最高,实验第30天时毒素残留量高达62.4%;PSTs引发栉孔扇贝体内脂质过氧化,过氧化物酶(POD)、超氧化物歧化酶(SOD)及谷胱甘肽过氧化物酶(GSH-Px)显著应激(P<0.05)。透射电镜下观察组织病变,发现空泡化、染色质聚集和核质固缩等结构损伤。通过加权基因共表达网络分析鉴定细胞凋亡和谷胱甘肽代谢解毒通路显著应激上调,映射ALOX5、Af GST-σ11、caspase-8及Bax 4个关键转录因子。综上可知,除抗氧化应激外,栉孔扇贝可激活特征性细胞凋亡和以谷胱甘肽解毒代谢反应抵抗PSTs毒性作用。本研究可为深入探索栉孔扇贝应激与代谢PSTs的特征机制提供科学依据。Paralytic shellfish toxins(PSTs)are some of the most harmful algal neurotoxins in the world.They easily accumulate in bivalve shellfish and are transmitted through the food chain,causing symptoms such as nausea and vomiting,muscle paralysis,dyspnea and even asphyxiation in consumers,leading to food poisoning in humans.Therefore,a widely accepted limit standard of 800μg STXeq/kg has been established as a safe limit for PSTs.PSTs are produced by some microalgae,among which Alexandrium tamarense is one of the predominant toxic algae found along the coast of China.It was found that the detection rate and over-standard rate of Chlamys farreri in bivalve shellfish sold in China are relatively high.PSTs are mainly stored in visceral masses and are characterized by their fast accumulation and slow metabolism.PSTs are neurotoxins that exert their toxic effects by blocking sodium channels and inhibiting nerve conduction.Studies have shown that PSTs can cause stress responses in bivalves,including production of a large amount of reactive oxygen species(ROS),antioxidant stress(including enzymatic and non-enzymatic defense),imbalance of intracellular redox homeostasis,and cell damage(i.e.,lipid peroxidation).As one of the main products of lipid peroxidation,the content of malondialdehyde(MDA)can directly reflect tissue and cell membrane damage caused by PSTs.In addition,superoxide dismutase(SOD)and peroxidase(POD)are often used as indicators to evaluate the level of antioxidation,and glutathione peroxidase(GSH-Px)plays a key role in antioxidant defense.The changes in lipid peroxidation and antioxidant enzymes are commonly used in existing studies to reflect the injury and degree of stress in organisms.Some studies have also shown that PSTs can cause tissue damage and induce abnormal gene expression in C.farreri,but research on the changes of gene expression and regulatory mechanism of PST-induced tissue damage in C.farreri is still lacking.This information is important for establishing and perfecting food safety risk assessm
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