Copper-induced sublethal effects in Bufo gargarizans tadpoles: growth, intestinal histology and microbial alternations

Zheng, Rui; Wu, Minyao; Wang, Hongyuan; Chai, Lihong; Peng, Jufang

doi:10.1007/s10646-021-02356-y

Cited by 12 publications

(1 citation statement)

References 69 publications

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“…In contrast, larval amphibians are known to actively drink water, providing a mechanism for Cu exposure to the gastrointestinal tract. Although not studied extensively, two studies have observed intestinal lesions, including disordered enterocytes, and abnormal villi and vacuoles in tadpoles exposed to Cu at concentrations (32–64 µg L −1 Cu) that elicit reduced tadpole growth (Yang et al, 2020 ; Zheng et al, 2021 ). These types of histological effects may be the result of oxidative stress from Cu exposure, although direct measurements of the oxidative status of the intestine were not made (Figure 2 ).…”

Section: Oxidative Stressmentioning

confidence: 99%

Adverse Outcome Pathways for Chronic Copper Toxicity to Fish and Amphibians

Brix

Boeck

Baken

et al. 2022

Enviro Toxic and Chemistry

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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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Section: Oxidative Stressmentioning

confidence: 99%