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Recovery of Alexandrium tamarense under chronic exposure of TiO2 nanoparticles and possible mechanisms

机译:TiO2纳米颗粒的慢性暴露下亚历山大仙群的回收及可能的机制

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摘要

Harmful algal blooms (HAB), heavily influenced by human activities, pose serious hazard to aquatic ecology and human health. In this study, we monitored the physiological responses and paralytic shellfish poisoning toxins (PSTs) of the toxin-producing HAB species Alexandrium tamarense under titanium dioxide nanoparticles (nTiO2) exposure in the concentration range of 2-320 mg L-1 over a period of 13 days. The results showed the acute inhibition of nTiO2 on the algal growth, photosynthetic efficiency and esterase activity at all concentrations except 2 mg L-1. Nonetheless, they recovered after 13 days nTiO2 exposure from 20 to 80 mg L-1. The EC50 value increased from 85.1 mg L-1 in Day 4 to 140.9 mg L-1 in Day 13. The physiological recovery after prolonged exposure may result from the elimination of excess reactive oxygen species (ROS), a combined outcome of increased nTiO2 aggregation and algal antioxidant defense mechanisms. This observation is supported by the immediately increased antioxidant enzyme activities, including the superoxide dismutase (SOD) and catalase (CAT) activities upon nTiO2 exposure. Moreover, the production of PSTs in A. tamarense significantly increased by 1.41-1.76 folds after chronic nTiO2 exposure at all tested concentrations (p & 0.05), which might also be an adaptive response for the microalgae to overcome the stresses. In particular, the proportions of highly-toxic PSTs analogues GTX2/3, STX and dcSTX were significantly increased upon nTiO2 exposure (p & 0.05). Hence, the chronic nTiO2 exposure might aggravate the ecological impact of HABs. Furthermore investigations on different HAB species, especially those toxin-producing ones, and detail physiological responses are obviously needed.
机译:有害的藻类绽放(HAB),受人活动的严重影响,对水生生态和人类健康构成严重危害。在这项研究中,我们在二氧化钛纳米粒子(NTIO2)暴露于2-320mg L-1的浓度范围内13天。结果表明,除2mg L-1之外的所有浓度下的藻类生长,光合效率和酯酶活性的急性抑制作用。尽管如此,它们在13天的NTIO2暴露于20至80mg L-1后回收。 EC50值在第13天的第4天至140.9mg L-1中增加到85.1mg L-1。延长曝光后的生理恢复可能是由于消除过量的反应性氧(ROS),而NTIO2聚集增加的组合结果和藻类抗氧化防御机制。该观察结果由立即增加的抗氧化酶活性,包括在NTIO2暴露中的超氧化物歧化酶(SOD)和过氧化氢酶(猫)活性。此外,在所有测试浓度(P& 0.05)的慢性NTIO2暴露后,胎塞在A.的PSTS的生产显着增加1.41-1.76倍,这也可能是微藻克服应力的适应性响应。特别地,在NTIO2暴露(P& 0.05)上显着增加了高毒性PSTS类似物GTX2 / 3,STX和DCSTX的比例显着增加。因此,慢性NTIO2暴露可能会加剧HABS的生态影响。此外,对不同HAB物种的研究,特别是那些产生毒素的生产和细节生理反应。

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