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渗出液混合物:探寻一种入侵性海藻对海洋无脊椎动物的毒性作用机制

Exudate Cocktail: The Quest for the Mechanisms of Toxic Action of an Invasive Seaweed on Marine Invertebrates.

作者信息

Silva Carla O, Simões Tiago, Félix Rafael, Soares Amadeu M V M, Barata Carlos, Novais Sara C, Lemos Marco F L

机构信息

MARE-Marine and Environmental Sciences Centre, ESTM, Instituto Politécnico de Leiria, 2520-641 Peniche, Portugal.

Department of Biology and CESAM (Centre for Environmental and Marine Studies), University of Aveiro, 3810-193 Aveiro, Portugal.

出版信息

Biology (Basel). 2021 Mar 14;10(3):223. doi: 10.3390/biology10030223.

Abstract

The seaweed exhibits a strong invasive behavior, producing halogenated compounds with effective biological effects. This study addresses the biochemical responses to sublethal concentrations of exudate on the marine snail whole body and the shrimp eyes and hepatopancreas. Antioxidant defenses superoxide dismutase (SOD) and glutathione-S-transferase (GST), oxidative damage endpoints lipid peroxidation (LPO) and DNA damage, the neuronal parameter acetylcholinesterase (AChE), and the fatty acid profile were evaluated. Results revealed different metabolic responses in both species. Despite previous studies indicating that the exudate affected survival and behavior, this does not seem to result from oxidative stress or neurotoxicity. For , the inhibition of AChE and the decrease of antioxidant capacity is concomitant with the increase of LPO, suggesting neurotoxicity and oxidative stress as contributor mechanisms of toxicity for this species. Fatty acid profile changes were more pronounced for with a general increase in polyunsaturated fatty acids (PUFAs) with the exudate exposure, which commonly means a defense mechanism protecting from membrane disruption. Nonetheless, the omega-3 PUFAs arachidonic acid (ARA) and docosapentaenoic acid (DPA) increased in both invertebrates, indicating a common regulation mechanism of inflammation and immunity responses.

摘要

这种海藻表现出强烈的入侵行为,会产生具有有效生物效应的卤代化合物。本研究探讨了亚致死浓度的渗出物对海蜗牛全身以及虾的眼睛和肝胰腺的生化反应。评估了抗氧化防御超氧化物歧化酶(SOD)和谷胱甘肽 - S - 转移酶(GST)、氧化损伤终点脂质过氧化(LPO)和DNA损伤、神经参数乙酰胆碱酯酶(AChE)以及脂肪酸谱。结果显示两种物种有不同的代谢反应。尽管先前的研究表明渗出物会影响生存和行为,但这似乎并非由氧化应激或神经毒性导致。对于[此处原文缺失具体物种名称],AChE的抑制和抗氧化能力的降低与LPO的增加同时出现,表明神经毒性和氧化应激是该物种毒性的促成机制。随着渗出物暴露,[此处原文缺失具体物种名称]的脂肪酸谱变化更为明显,多不饱和脂肪酸(PUFA)普遍增加,这通常意味着一种防止膜破坏的防御机制。尽管如此,两种无脊椎动物中的ω - 3多不饱和脂肪酸花生四烯酸(ARA)和二十二碳五烯酸(DPA)都增加了,表明存在炎症和免疫反应的共同调节机制。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/aee0/8002046/5337bf36634f/biology-10-00223-g001.jpg

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