Progress in Understanding Algal Bloom-Mediated Fish Kills: The Role of Superoxide Radicals, Phycotoxins and Fatty Acids.
Progress in Understanding Algal Bloom-Mediated Fish Kills: The Role of Superoxide Radicals, Phycotoxins and Fatty Acids.
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DOI：
10.1371/journal.pone.0133549
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发表时间：
2015
期刊：
影响因子：
3.7
通讯作者：
Hallegraeff GM
中科院分区：
文献类型：
--
作者：
Dorantes-Aranda JJ;Seger A;Mardones JI;Nichols PD;Hallegraeff GM
对活性氧、藻毒素和脂肪酸在有害海洋微藻对鱼类毒性中的作用进行量化仍无定论。采用离体鱼鳃法同时测定了7种鱼毒微藻（Chattonella marina、Fibrocapsa japonica、Heterosigma akashiwo、Karenia mikimotoi、Alexandrium catenella、Karlodinium veneficum、Prymnesium parvum）对超氧化物歧化酶（SOD）、过氧化氢酶（CAT）和乳酸脱氢酶（LDH）活性的影响。还对这些藻类产生的超氧化物进行了定量。比较了纯化藻毒素和粗提物的效果，并讨论了脂肪酸的影响。针形藻Chattonella是最鱼毒性（鳃细胞活力下降到35%），也是超氧自由基（14 pmol细胞-1小时-1），特别是细胞裂解后的主要生产者。针形藻异弯藻和甲藻亚历山大藻的毒性最小，且产生的超氧化物较少。裂解链状体（5.6 μ mol细胞-1hr-1）。过氧化氢酶活性在所有处理中均无变化。超氧化物歧化酶（SOD）和乳酸脱氢酶（LDH）活性分别比对照组增加≤23%和51.2%。码头，但剩余藻类的SOD变化不明显。鳃细胞活力和超氧化物产生或超氧化物歧化酶之间没有观察到很强的关系。纯化的短鞭藻毒素PbTx-2和PbTx-3（来自短凯伦藻，LC 50为22.1 μg mL-1对35.2 μg mL-1）和karlotoxin KmTx-2（来自Karlodinium; LC 50 = 380 ng mL-1）几乎可以完全解释这两种甲藻的杀鱼活性。然而，麻痹性贝类毒素（PST）GTX 1和4，C1和C2，和STX没有解释亚历山大鱼毒性。只有亚历山大藻的水提取物具有细胞毒性（存活率降低≤65%），而查顿藻、纤维囊藻、异弯藻、卡甲藻和Prymnesium的粗甲醇和丙酮提取物使细胞存活率降低至0%。这些和我们以前的研究结果涉及脂肪酸的作用证实，超氧自由基只部分参与鱼类毒性，并指出一个高度可变的贡献，由其他化合物，如脂质过氧化产物（如醛）。
Quantification of the role of reactive oxygen species, phycotoxins and fatty acids in fish toxicity by harmful marine microalgae remains inconclusive. An in vitro fish gill (from rainbow trout Oncorhynchus mykiss) assay was used to simultaneously assess the effect in superoxide dismutase, catalase and lactate dehydrogenase enzymatic activities caused by seven species of ichthyotoxic microalgae (Chattonella marina, Fibrocapsa japonica, Heterosigma akashiwo, Karenia mikimotoi, Alexandrium catenella, Karlodinium veneficum, Prymnesium parvum). Quantification of superoxide production by these algae was also performed. The effect of purified phycotoxins and crude extracts was compared, and the effect of fatty acids is discussed. The raphidophyte Chattonella was the most ichthyotoxic (gill cell viability down to 35%) and also the major producer of superoxide radicals (14 pmol cell-1 hr-1) especially after cell lysis. The raphidophyte Heterosigma and dinoflagellate Alexandrium were the least toxic and had low superoxide production, except when A. catenella was lysed (5.6 pmol cell-1 hr-1). Catalase showed no changes in activity in all the treatments. Superoxide dismutase (SOD) and lactate dehydrogenase exhibited significant activity increases of ≤23% and 51.2% TCC (total cellular content), respectively, after exposure to C. marina, but SOD showed insignificant changes with remaining algal species. A strong relationship between gill cell viability and superoxide production or superoxide dismutase was not observed. Purified brevetoxins PbTx-2 and -3 (from Karenia brevis, LC50 of 22.1 versus 35.2 μg mL-1) and karlotoxin KmTx-2 (from Karlodinium; LC50 = 380 ng mL-1) could almost entirely account for the fish killing activity by those two dinoflagellates. However, the paralytic shellfish toxins (PST) GTX1&4, C1&C2, and STX did not account for Alexandrium ichthyotoxicity. Only aqueous extracts of Alexandrium were cytotoxic (≤65% decrease of viability), whereas crude methanol and acetone extracts of Chattonella, Fibrocapsa, Heterosigma, Karlodinium and Prymnesium decreased cell viability down to 0%. These and our previous findings involving the role of fatty acids confirm that superoxide radicals are only partially involved in ichthyotoxicity and point to a highly variable contribution by other compounds such as lipid peroxidation products (e.g. aldehydes).