Adverse Outcome Pathways for Chronic Copper Toxicity to Fish and Amphibians

Kevin V. Brix; Gudrun De Boeck; Stijn BakenDouglas J. Fort

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Adverse Outcome Pathways for Chronic Copper Toxicity to Fish and Amphibians

机译：Adverse Outcome Pathways for Chronic Copper Toxicity to Fish and Amphibians

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In the present review, we synthesize information on the mechanisms of chronic copper (Cu) toxicity using an adverse outcome pathway framework and identify three primary pathways for chronic Cu toxicity: disruption of sodium homeostasis, effects on bioenergetics, and oxidative stress. Unlike acute Cu toxicity, disruption of sodium homeostasis is not a driving mechanism of chronic toxicity, but compensatory responses in this pathway contribute to effects on organism bioenergetics. Effects on bioenergetics clearly contribute to chronic Cu toxicity with impacts at multiple lower levels of biological organization. However, quantitatively translating these impacts into effects on apical endpoints such as growth, amphibian metamorphosis, and reproduction remains elusive and requires further study. Copper‐induced oxidative stress occurs in most tissues of aquatic vertebrates and is clearly a significant driver of chronic Cu toxicity. Although antioxidant responses and capacities differ among tissues, there is no clear indication that specific tissues are more sensitive than others to oxidative stress. Oxidative stress leads to increased apoptosis and cellular damage in multiple tissues, including some that contribute to bioenergetic effects. This also includes oxidative damage to tissues involved in neuroendocrine axes and this damage likely alters the normal function of these tissues. Importantly, Cu‐induced changes in hormone concentrations and gene expression in endocrine‐mediated pathways such as reproductive steroidogenesis and amphibian metamorphosis are likely the result of oxidative stress‐induced tissue damage and not endocrine disruption. Overall, we conclude that oxidative stress is likely the primary driver of chronic Cu toxicity in aquatic vertebrates, with bioenergetic effects and compensatory response to disruption of sodium homeostasis contributing to some degree to observed effects on apical endpoints.

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《Environmental toxicology and chemistry /》 |2022年第12期|2911-2927|共17页
作者
Kevin V. Brix; Gudrun De Boeck; Stijn BakenDouglas J. Fort;
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作者单位

EcoTox, Miami, Florida, USA,Rosenstiel School of Marine, Atmospheric, and Earth Sciences, Department of Marine Biology and Ecology, University of Miami, Miami, Florida, USA;

Department of Biology, University of Antwerp, Antwerp, Belgium;

European Copper Institute, Brussels, BelgiumFort Environmental Labs, Stillwater, Oklahoma, USA;

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收录信息美国《科学引文索引》(SCI);美国《工程索引》(EI);美国《生物学医学文摘》(MEDLINE);美国《化学文摘》(CA);
原文格式 PDF
正文语种英语
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Adverse outcome pathway; copper; endocrine disruption; mode of action; oxidative stress;

Adverse Outcome Pathways for Chronic Copper Toxicity to Fish and Amphibians

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