Reshma Kalarical Janardhanan, Milen Nachev, Bernd Sures, Inna M Sokolova
{"title":"低氧胁迫改变蓝贻贝对亚致死铜暴露的反应而不诱导交叉耐受。","authors":"Reshma Kalarical Janardhanan, Milen Nachev, Bernd Sures, Inna M Sokolova","doi":"10.1016/j.aquatox.2025.107523","DOIUrl":null,"url":null,"abstract":"<p><p>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.</p>","PeriodicalId":248,"journal":{"name":"Aquatic Toxicology","volume":"287 ","pages":"107523"},"PeriodicalIF":4.3000,"publicationDate":"2025-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"Low oxygen stress alters response to sublethal copper exposure without inducing cross-tolerance in the blue mussel Mytilus edulis.\",\"authors\":\"Reshma Kalarical Janardhanan, Milen Nachev, Bernd Sures, Inna M Sokolova\",\"doi\":\"10.1016/j.aquatox.2025.107523\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><p>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.</p>\",\"PeriodicalId\":248,\"journal\":{\"name\":\"Aquatic Toxicology\",\"volume\":\"287 \",\"pages\":\"107523\"},\"PeriodicalIF\":4.3000,\"publicationDate\":\"2025-10-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Aquatic Toxicology\",\"FirstCategoryId\":\"93\",\"ListUrlMain\":\"https://doi.org/10.1016/j.aquatox.2025.107523\",\"RegionNum\":2,\"RegionCategory\":\"环境科学与生态学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"2025/8/5 0:00:00\",\"PubModel\":\"Epub\",\"JCR\":\"Q1\",\"JCRName\":\"MARINE & FRESHWATER BIOLOGY\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Aquatic Toxicology","FirstCategoryId":"93","ListUrlMain":"https://doi.org/10.1016/j.aquatox.2025.107523","RegionNum":2,"RegionCategory":"环境科学与生态学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2025/8/5 0:00:00","PubModel":"Epub","JCR":"Q1","JCRName":"MARINE & FRESHWATER BIOLOGY","Score":null,"Total":0}
Low oxygen stress alters response to sublethal copper exposure without inducing cross-tolerance in the blue mussel Mytilus edulis.
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.
期刊介绍:
Aquatic Toxicology publishes significant contributions that increase the understanding of the impact of harmful substances (including natural and synthetic chemicals) on aquatic organisms and ecosystems.
Aquatic Toxicology considers both laboratory and field studies with a focus on marine/ freshwater environments. We strive to attract high quality original scientific papers, critical reviews and expert opinion papers in the following areas: Effects of harmful substances on molecular, cellular, sub-organismal, organismal, population, community, and ecosystem level; Toxic Mechanisms; Genetic disturbances, transgenerational effects, behavioral and adaptive responses; Impacts of harmful substances on structure, function of and services provided by aquatic ecosystems; Mixture toxicity assessment; Statistical approaches to predict exposure to and hazards of contaminants
The journal also considers manuscripts in other areas, such as the development of innovative concepts, approaches, and methodologies, which promote the wider application of toxicological datasets to the protection of aquatic environments and inform ecological risk assessments and decision making by relevant authorities.