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Glutathione Transferase Activity And Oocyte Development In Copepods Exposed To Toxic Phytoplankton

机译:暴露于有毒浮游植物的Co足类动物谷胱甘肽转移酶活性和卵母细胞发育

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Organisms present a series of cellular mechanisms to avoid the effects of toxic compounds. Such mechanisms include the increase in activity of detoxification enzymes [e.g., 7-ethoxyresorufin-O-deethylase (EROD) and glutathione S-transferase (GST)], which could explain the low retention of ingested toxins generally observed in copepods. In addition, decreasing gross growth efficiency (GGE) of copepods with increasing concentration of toxic diets could be caused either by a high expenditure coping with toxins (e.g., increase in the activity of detoxification enzymes) or by a deterioration of reproductive tissues. To assess the effect of toxic phytoplankton on the activity of detoxification enzymes and on oocyte maturation of Acartia tonsa and Temora longicornis, feeding and egg production experiments were carried out with a variety of toxic diets and an adequate non-toxic food control (Rhodomonas spp.) all provided as single species diets. Toxic diets included the nodularin-producing cyanobacterium Nodularia spumigena, the dinoflagellates Alexandrium minutum, and A. tamarense, which contained Paralytic Shellfish Poisoning (PSP) toxins, the dinoflagellate Prorocentrum lima with Diarrhetic Shellfish Poisoning (DSP) toxins and the haptophyte Prymnesium parvum, which produces ichtyotoxins with haemolytic activity. Feeding on toxic diets was lower than on Rhodomonas spp., except for A. minutum and A. tamarense. In addition, toxic diets negatively affected reproduction in both copepod species with the production of oocytes and oocyte development impaired with A. minutum and N. spumigena. While the negative effect of N. spumigena seemed to be connected to gonad atresia likely caused by severe food limitation (starvation), the negative effect of A. minutum could have been either caused by a direct effect of saxitoxins or nutritional inadequacy on oocyte production. We could not detect EROD activity in the copepods, while the activity of GST was generally higher with the non-toxic food control and positively related to the feeding and egestion rates, suggesting relation to feeding conditions rather than to exposure to toxic diets. No relationship was found between GGE and GST activity. Our results refute the hypothesis that toxic diets, provided at ecologically relevant levels, would induce cellular mechanisms in copepods regarding GST activity. GST activity thus seems to play no role in detoxification of copepods confronted with toxic phytoplankton. Toxin detoxification and its cost for copepods still remain an open question.
机译:生物提出了一系列细胞机制来避免有毒化合物的影响。此类机制包括解毒酶[例如7-乙氧基间苯二酚-O-脱乙基酶(EROD)和谷胱甘肽S-转移酶(GST)]的活性增加,这可以解释在co足类动物中通常观察到的摄入的毒素保留率较低。另外,with足类动物的总生长效率(GGE)随着有毒食物浓度的增加而降低,可能是由于高剂量的毒素应对(例如,解毒酶活性的提高)或生殖组织的恶化引起的。为了评估有毒浮游植物对解毒酶活性以及A螨和长尾em(Temora longicornis)卵母细胞成熟的影响,采用多种有毒饮食和适当的无毒食物控制进行了摄食和产蛋实验(Rhodomonas spp。 )全部以单一物种饮食提供。有毒的饮食包括产生结节菌素的蓝藻结节菌Nodularia spumigena,小鞭毛亚历山大藻(Alexandreminutum)和tamarense.A。tamarense,其中含有麻痹性贝类毒素(PSP)毒素,带鞭毛的腹泻性原鞭毛虫利马和腹泻性贝类毒素(DSP)以及拟南芥产生具有溶血活性的鱼腥毒素。除了小菜曲霉和塔玛森曲霉以外,有毒饮食的摄食量低于红假单胞菌。此外,有毒饮食对两种co足类物种的繁殖均产生负面影响,卵母细胞的产生和细小曲霉和产孢杆菌的卵母细胞发育受到损害。虽然可能是由于严重的食物限制(饥饿)引起的,产孢杆菌的负面影响可能与性腺闭锁有关,但细孢曲霉的负面影响可能是由毒素引起的直接作用或营养不足对卵母细胞产生造成的。我们无法在the足类动物中检测到EROD活性,而在无毒食品控制中,GST的活性通常较高,并且与摄食率和节食率呈正相关,表明与摄食条件有关,而不是与有毒饮食接触。在GGE和GST活性之间未发现任何关系。我们的研究结果驳斥了这样的假设:有毒的饮食(在生态上相关的水平)会诱导co足类中有关GST活性的细胞机制。因此,GST活性似乎在面对有毒浮游植物的co足类动物的解毒中不起作用。毒素排毒及其对co足类的成本仍然是一个未解决的问题。

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