A generic biotic ligand model quantifying the development in time of Ni toxicity to Enchytraeus crypticus

He, Erkai; Qiu, Hao; Dimitrova, Katya; Gestel, Cornelis A.M. van

doi:10.1016/j.chemosphere.2014.12.034

Cited by 7 publications

(5 citation statements)

References 38 publications

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“…It is obvious that at high metal concentrations, the toxicity becomes less specific (metal binding to low-affinity sites once the high-affinity sites are occupied). However, a very recent study on Ni 2+ toxicity showed that on the basis of biotic ligand models, chronic toxicity cannot be predicted by models for acute toxicity, 232 confirming earlier studies on zooplankton with other metals. To unravel the mechanisms of metal toxicity, it is important to study the effects under environmentally relevant conditions to ensure a specific effect and not an overall inhibition of the metabolism.…”

Section: Discussionsupporting

confidence: 64%

Mechanisms of metal toxicity in plants

2016

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Metal toxicity in plants is still a global problem for the environment, agriculture and ultimately human health. This review initially addresses the current state of the environmental/agricultural problem, and then discusses in detail the occurrence, mechanisms and relevance of toxicity of selected trace metals (Cd, Cu, Fe, Hg, Ni, and Zn). When discussing the mechanisms, special emphasis is laid on a critical review of their environmental/agricultural relevance, because even now many studies in this field of research are performed under highly artificial lab conditions. The main problems outlined in published studies are artificially high metal concentrations (which never occur even in highly polluted sites) combined with too short treatment times, as well as environmentally and agriculturally irrelevant growth conditions (e.g. constant light and submerged cultivation of seedlings). Furthermore, wherever possible an attempt is made to link the mechanisms published to date in terms of discussing which mechanisms are a direct cause of the observed disturbance of plant function and which are rather a consequence of the primary mechanisms, leading to a complicated toxicity phenotype and ultimately to diminished growth or even death of the plants.

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Section: Discussionsupporting

confidence: 64%

Mechanisms of metal toxicity in plants

2016

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“…At the whole‐animal level, a negative relationship between increasing water hardness (Ca 2+ and Mg 2+ ) and metal toxicity to aquatic organisms has been well documented for over 30 yr for a number of divalent metals including Ni . In some cases, these relationships may have been confounded by other covarying water quality parameters such as alkalinity and pH because of the specific ionic composition of natural and synthetic waters, but subsequent ion‐specific studies have confirmed that increasing ambient Ca 2+ reduces both acute and chronic Ni toxicity to a variety of aquatic and terrestrial animals . In contrast, most studies indicate that Ca 2+ has no effect on Ni toxicity to aquatic or terrestrial plants, suggesting that Ni uptake occurs via different mechanisms in plants .…”

Section: Disruption Of Ca2+ Homeostasismentioning

confidence: 99%

“…Similar to Ca 2+ , at the whole‐animal level there is an abundance of data showing that Mg 2+ reduces Ni accumulation and toxicity in a variety of organisms. Increasing waterborne Mg 2+ concentrations reduce Ni toxicity to daphnids , oligochaetes , rainbow trout , and frog embryos . Unlike Ca 2+ , ambient Mg 2+ also reduces Ni toxicity in terrestrial , but not aquatic , plants.…”

Section: Disruption Of Mg2+ Homeostasismentioning

confidence: 99%

The mechanisms of nickel toxicity in aquatic environments: An adverse outcome pathway analysis

Brix

Schlekat²,

Garman³

2017

Enviro Toxic and Chemistry

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Current ecological risk assessment and water quality regulations for nickel (Ni) use mechanistically based, predictive tools such as biotic ligand models (BLMs). However, despite many detailed studies, the precise mechanism(s) of Ni toxicity to aquatic organisms remains elusive. This uncertainty in the mechanism(s) of action for Ni has led to concern over the use of tools like the BLM in some regulatory settings. To address this knowledge gap, the authors used an adverse outcome pathway (AOP) analysis, the first AOP for a metal, to identify multiple potential mechanisms of Ni toxicity and their interactions with freshwater aquatic organisms. The analysis considered potential mechanisms of action based on data from a wide range of organisms in aquatic and terrestrial environments on the premise that molecular initiating events for an essential metal would potentially be conserved across taxa. Through this analysis the authors identified 5 potential molecular initiating events by which Ni may exert toxicity on aquatic organisms: disruption of Ca 2þ homeostasis, disruption of Mg 2þ homeostasis, disruption of Fe 2þ/3þ homeostasis, reactive oxygen species-induced oxidative damage, and an allergic-type response of respiratory epithelia. At the organ level of biological organization, these 5 potential molecular initiating events collapse into 3 potential pathways: reduced Ca 2þ availability to support formation of exoskeleton, shell, and bone for growth; impaired respiration; and cytotoxicity and tumor formation. At the level of the whole organism, the organ-level responses contribute to potential reductions in growth and reproduction and/or alterations in energy metabolism, with several potential feedback loops between each of the pathways. Overall, the present AOP analysis provides a robust framework for future directed studies on the mechanisms of Ni toxicity and for developing AOPs for other metals.

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“…In contrast, studies indicate Ca 2+ has no effect on nickel toxicity to aquatic or terrestrial plants, suggesting nickel uptake occurs via different mechanisms in plants [223]. Additionally, increasing Mg 2+ concentration reduces Ni accumulation and toxicity in a variety of organisms (daphnids, oligochaetes, rainbow trout, and frog embryos) [167,173,224,225]. Increasing Mg 2+ also reduces nickel toxicity in terrestrial [170] but not aquatic plants [226].…”

Section: Mechanisms Of Toxicitymentioning

confidence: 99%

Concise Review of Nickel Human Health Toxicology and Ecotoxicology

Buxton¹,

Garman²,

Heim³

et al. 2019

Inorganics

157

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Nickel (Ni) metal and Ni compounds are widely used in applications like stainless steel, alloys, and batteries. Nickel is a naturally occurring element in water, soil, air, and living organisms, and is essential to microorganisms and plants. Thus, human and environmental nickel exposures are ubiquitous. Production and use of nickel and its compounds can, however, result in additional exposures to humans and the environment. Notable human health toxicity effects identified from human and/or animal studies include respiratory cancer, non-cancer toxicity effects following inhalation, dermatitis, and reproductive effects. These effects have thresholds, with indirect genotoxic and epigenetic events underlying the threshold mode of action for nickel carcinogenicity. Differences in human toxicity potencies/potentials of different nickel chemical forms are correlated with the bioavailability of the Ni2+ ion at target sites. Likewise, Ni2+ has been demonstrated to be the toxic chemical species in the environment, and models have been developed that account for the influence of abiotic factors on the bioavailability and toxicity of Ni2+ in different habitats. Emerging issues regarding the toxicity of nickel nanoforms and metal mixtures are briefly discussed. This review is unique in its covering of both human and environmental nickel toxicity data.

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A generic biotic ligand model quantifying the development in time of Ni toxicity to Enchytraeus crypticus

Cited by 7 publications

References 38 publications

Mechanisms of metal toxicity in plants

Mechanisms of metal toxicity in plants

The mechanisms of nickel toxicity in aquatic environments: An adverse outcome pathway analysis

Concise Review of Nickel Human Health Toxicology and Ecotoxicology

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