globalchange  > 气候减缓与适应
DOI: 10.1016/j.envpol.2018.11.020
WOS记录号: WOS:000457511900046
论文题名:
Bioaccumulation and ecotoxicological responses of juvenile white seabream (Diplodus sargus) exposed to triclosan, warming and acidification
作者: Maulvault, Ana Luisa1,2,3; Camacho, Carolina1,2; Barbosa, Vera1,2; Alves, Ricardo1; Anacleto, Patricia1,2,3; Cunha, Sara C.4; Fernandes, Jose O.4; Pousao-Ferreira, Pedro1; Paula, Jose Ricardo3; Rosa, Rui3; Diniz, Mario5; Marques, Antonio1,2
通讯作者: Maulvault, Ana Luisa
刊名: ENVIRONMENTAL POLLUTION
ISSN: 0269-7491
EISSN: 1873-6424
出版年: 2019
卷: 245, 页码:427-442
语种: 英语
英文关键词: Triclosan ; Bioaccumulation ; Warming ; Acidification ; Multi-biomarkers responses
WOS关键词: BASS DICENTRARCHUS-LABRAX ; OCEAN ACIDIFICATION ; ECOPHYSIOLOGICAL RESPONSES ; ENZYME-ACTIVITIES ; OXIDATIVE STRESS ; GENE-EXPRESSION ; CLIMATE-CHANGE ; ENERGY BUDGET ; SEA BREAM ; FISH
WOS学科分类: Environmental Sciences
WOS研究方向: Environmental Sciences & Ecology
英文摘要:

Triclosan (TCS) is a synthetic microbial compound widely used in the formulation of various personal care products. Its frequent detection in marine ecosystems, along with its physical and chemical properties, suggest that TCS can be highly persistent, being easily bioaccumulated by biota and, therefore, eliciting various toxicological responses. Yet, TCS's mechanisms of bioaccumulation and toxicity still deserve further research, particularly focusing on the interactive effects with climate change-related stressors (e.g. warming and acidification), as both TCS chemical behaviour and marine species metabolism/physiology can be strongly influenced by the surrounding abiotic conditions. Hence, the aim of this study was to assess TCS bioaccumulation and ecotoxicological effects (i.e. animal fitness indexes, antioxidant activity, protein chaperoning and degradation, neurotoxicity and endocrine disruption) in three tissues (i.e. brain, liver and muscle) of juvenile Diplodus sargus exposed to the interactive effects of TCS dietary exposure (15.9 mu g kg(-1) dw), seawater warming (Delta T degrees C = +5 degrees C) and acidification (Delta pCO(2) similar to +1000 mu atm, equivalent to Delta pH = -0.4 units). Muscle was the primary organ of TCS bioaccumulation, and climate change stressors, particularly warming, significantly reduced TCS bioaccumulation in all fish tissues. Furthermore, the negative ecotoxicological responses elicited by TCS were significantly altered by the co-exposure to acidification and/or warming, through either the enhancement (e.g. vitellogenin content) or counteraction/inhibition (e.g. heat shock proteins HSP70/HSC70 content) of molecular biomarker responses, with the combination of TCS plus acidification resulting in more severe alterations. Thus, the distinct patterns of TCS tissue bioaccumulation and ecotoxicological responses induced by the different scenarios emphasized the need to further understand the interactive effects between pollutants and abiotic conditions, as such knowledge enables a better estimation and mitigation of the toxicological impacts of climate change in marine ecosystems. (C) 2018 Elsevier Ltd. All rights reserved.


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资源类型: 期刊论文
标识符: http://119.78.100.158/handle/2HF3EXSE/128657
Appears in Collections:气候减缓与适应

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作者单位: 1.Portuguese Inst Sea & Atmosphere, Div Aquaculture & Seafood Upgrading, IP IPMA, Rua Alfredo Magalhaes Ramalho 6, P-1495006 Lisbon, Portugal
2.Univ Porto, Interdisciplinary Ctr Marine & Environm Res CIIMA, Ave Gen Norton de Matos S-N, P-4450208 Matosinhos, Portugal
3.Univ Lisbon, MARE Marine & Environm Sci Ctr, Lab Maritimo Guia, Fac Ciencias, Av Nossa Senhora Cabo 939, P-2750374 Cascais, Portugal
4.Univ Porto, Fac Pharm, LAQV REQUIMTE, Lab Bromatol & Hydrol, Porto, Portugal
5.Univ NOVA Lisboa, Fac Ciencias & Tecnol, Dept Chem, UCIBIO REQUIMTE, P-2829516 Caparica, Portugal

Recommended Citation:
Maulvault, Ana Luisa,Camacho, Carolina,Barbosa, Vera,et al. Bioaccumulation and ecotoxicological responses of juvenile white seabream (Diplodus sargus) exposed to triclosan, warming and acidification[J]. ENVIRONMENTAL POLLUTION,2019-01-01,245:427-442
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