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低氧胁迫会改变紫贻贝对亚致死铜暴露的反应,且不会诱导其产生交叉耐受性。

Low oxygen stress alters response to sublethal copper exposure without inducing cross-tolerance in the blue mussel Mytilus edulis.

作者信息

Janardhanan Reshma Kalarical, Nachev Milen, Sures Bernd, Sokolova Inna M

机构信息

Department of Marine Biology, Institute for Biological Sciences, University of Rostock, Rostock, Germany.

Department of Aquatic Ecology and Centre of Water and Environmental Research (ZWU), University of Duisburg-Essen, Essen, Germany.

出版信息

Aquat Toxicol. 2025 Oct;287:107523. doi: 10.1016/j.aquatox.2025.107523. Epub 2025 Aug 5.

Abstract

The Baltic Sea's limited water exchange and densely populated catchment area contribute to the frequent co-occurrence of hypoxia and chemical pollutants such as copper (Cu), raising concerns about the effects of sequential stressors on marine organisms. This study tested whether pre-exposure to intermittent oxygen stress alters the physiological and immune responses of Mytilus edulis to subsequent Cu exposure. Mussels were preconditioned for 21 days to either mild intermittent hypoxia (7 h/day at ∼2 mg/L DO) or severe intermittent anoxia (2 days/week at <0.01 mg/L DO), followed by a 7-day exposure to sublethal Cu (20 µg/L) under normoxia. Hypoxia preconditioning impaired Cu homeostasis, leading to elevated Cu accumulation. Hypoxia-exposed mussels maintained immune function (phagocytosis, lysosomal integrity, acid phosphatase activity), while anoxia disrupted phagocyte-lysosome balance. Cu exposure alone reduced hemocyte abundance and increased acid phosphatase activity, indicating typical immunotoxic effects that were not alleviated by prior oxygen stress. Lipid reserves declined under both oxygen regimes, while carbohydrate and protein levels were reduced by hypoxia. Anoxia preconditioning mitigated Cu-induced energy depletion, as reflected by elevated lipid and carbohydrate levels. Mitochondrial electron transport system activity increased following low oxygen preconditioning and further during Cu exposure, suggesting elevated energy demands at post-stress recovery/detoxification. Despite these bioenergetic adjustments, oxidative stress markers (total antioxidant capacity, lipid peroxidation) and stress gene expression (hsp70, hsp90, GADD45A, nrf2, NfκB) remained stable across treatments. In conclusion, while oxygen stress modulated mussel responses to Cu, it did not confer cross-tolerance, highlighting the complex and context-dependent nature of multiple stressor interactions in coastal environments.

摘要

波罗的海有限的水体交换和人口密集的集水区导致缺氧和化学污染物(如铜)经常同时出现,引发了人们对连续应激源对海洋生物影响的担忧。本研究测试了预先暴露于间歇性氧应激是否会改变紫贻贝对随后铜暴露的生理和免疫反应。贻贝被预处理21天,分别处于轻度间歇性缺氧(每天7小时,溶解氧约2毫克/升)或严重间歇性缺氧(每周2天,溶解氧<0.01毫克/升),然后在常氧条件下暴露于亚致死剂量的铜(20微克/升)7天。缺氧预处理损害了铜的体内平衡,导致铜积累增加。暴露于缺氧环境的贻贝维持了免疫功能(吞噬作用、溶酶体完整性、酸性磷酸酶活性),而缺氧则破坏了吞噬细胞-溶酶体平衡。单独的铜暴露降低了血细胞丰度并增加了酸性磷酸酶活性,表明典型的免疫毒性作用并未因先前的氧应激而减轻。在两种氧条件下脂质储备均下降,而缺氧使碳水化合物和蛋白质水平降低。缺氧预处理减轻了铜诱导的能量消耗,这表现为脂质和碳水化合物水平升高。低氧预处理后线粒体电子传递系统活性增加,在铜暴露期间进一步增加,表明应激后恢复/解毒时能量需求增加。尽管有这些生物能量调节,但氧化应激标志物(总抗氧化能力、脂质过氧化)和应激基因表达(hsp70、hsp90、GADD45A、nrf2、NfκB)在各处理组中保持稳定。总之,虽然氧应激调节了贻贝对铜的反应,但并未赋予交叉耐受性,突出了沿海环境中多种应激源相互作用的复杂性和背景依赖性。

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