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pCO驱动的海水酸化影响幼体牙鲆(Paralichthys olivaceus)水相铜毒性:肝脏中的金属积累、抗氧化防御和解毒作用

pCO-driven seawater acidification affects aqueous-phase copper toxicity in juvenile flounder Paralichthys olivaceus: Metal accumulation, antioxidant defenses and detoxification in livers.

作者信息

Xiao Zitao, Cao Liang, Liu Jinhu, Cui Wenting, Dou Shuozeng

机构信息

CAS Key Laboratory of Marine Ecology and Environmental Sciences, Institute of Oceanology, Center for Ocean Mega-Science, Chinese Academy of Sciences, Qingdao 266071, China; University of Chinese Academy of Sciences, Beijing 100039, China.

CAS Key Laboratory of Marine Ecology and Environmental Sciences, Institute of Oceanology, Center for Ocean Mega-Science, Chinese Academy of Sciences, Qingdao 266071, China; Laboratory for Marine Ecology and Environmental Science, Qingdao National Laboratory for Marine Science and Technology, Qingdao 266071, China.

出版信息

Sci Total Environ. 2023 Feb 1;858(Pt 3):160040. doi: 10.1016/j.scitotenv.2022.160040. Epub 2022 Nov 5.

Abstract

Ocean acidification potentially influences the biotoxicity of metals and the antioxidant defense systems of marine organisms. This study investigated how pCO-driven seawater acidification (SA) affected aqueous-phase copper (Cu) toxicity in the juvenile flounder Paralichthys olivaceus from the perspective of hepatic oxidative stress and damage to better understand the mechanisms underlying the biological effects produced by the two stressors. Fish were exposed to aqueous-phase Cu at relevant ambient and polluted concentrations (0, 5, 10, 50, 100 and 200 μg L) at different pH levels (no SA: pH 8.10; moderate SA: pH 7.70, pCO ∼1353.89 μatm; extreme SA: pH 7.30, pCO ∼3471.27 μatm) for 28 days. A battery of biomarkers in the livers was examined to investigate their roles in antioxidant defense and detoxification in response to coexposure. Hepatic Cu accumulation (30.22-184.90 mg kg) was positively correlated with Cu concentrations. The biomarkers responded adaptively to different redox states following SA and Cu exposure. In unacidified seawater, increases in Cu concentrations significantly induced hepatic lipid peroxidation (LPO, by up to 27.03 %), although compensatory responses in antioxidant defenses and detoxification were activated. Moderate SA helped maintain hepatic redox homeostasis and alleviated LPO through different defense strategies, depending on Cu concentrations. Under extreme SA, antioxidant-based defenses were activated to cope with oxidative stress at ambient-low Cu concentrations but failed to defend against Cu toxicity at polluted Cu levels, and LPO (by up to 63.90 %) was significantly induced. Additionally, thiols (GSH and MT) responded actively to cope with Cu toxicity under SA. SOD, CAT, EROD, and GST were also sensitively involved in defending against hepatic oxidative stress during coexposure. These findings highlight the notable interactive effects of SA and Cu and provide a basis for understanding antioxidant-based defenses in marine fish confronting environmental challenges.

摘要

海洋酸化可能会影响金属的生物毒性以及海洋生物的抗氧化防御系统。本研究从肝脏氧化应激和损伤的角度,调查了由pCO驱动的海水酸化(SA)如何影响幼年牙鲆(Paralichthys olivaceus)水相铜(Cu)的毒性,以便更好地理解这两种应激源产生生物效应的潜在机制。将鱼暴露于不同pH水平(无SA:pH 8.10;中度SA:pH 7.70,pCO ∼1353.89 μatm;极端SA:pH 7.30,pCO ∼3471.27 μatm)下相关的环境和污染浓度(0、5、10、50、100和200 μg/L)的水相铜中28天。检测了肝脏中的一系列生物标志物,以研究它们在联合暴露时的抗氧化防御和解毒作用。肝脏铜积累量(30.22 - 184.90 mg/kg)与铜浓度呈正相关。在SA和铜暴露后,生物标志物对不同的氧化还原状态有适应性反应。在未酸化的海水中,铜浓度的增加显著诱导了肝脏脂质过氧化(LPO,最高可达27.03%),尽管抗氧化防御和解毒的补偿反应被激活。中度SA通过不同的防御策略有助于维持肝脏氧化还原稳态并减轻LPO,这取决于铜浓度。在极端SA条件下,基于抗氧化剂的防御在环境低铜浓度下被激活以应对氧化应激,但在污染铜水平下无法抵御铜毒性,并且LPO(最高可达63.90%)被显著诱导。此外,硫醇(GSH和MT)在SA条件下积极响应以应对铜毒性。超氧化物歧化酶(SOD)、过氧化氢酶(CAT)、乙氧基异吩唑酮 - O - 脱乙基酶(EROD)和谷胱甘肽 - S - 转移酶(GST)在联合暴露期间也敏感地参与抵御肝脏氧化应激。这些发现突出了SA和铜之间显著的交互作用,并为理解海洋鱼类面对环境挑战时基于抗氧化剂的防御提供了依据。

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