Passive transport pathways for Ca2+ and Co2+ in human red blood cells. 57Co2+ as a tracer for Ca2+ influx

Simonsen, Leif; Harbak, Henrik; Bennekou, Poul

doi:10.1016/j.bcmd.2011.09.002

Cited by 12 publications

(5 citation statements)

References 53 publications

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“…Hip implant-released Co has been associated with a number of severe adverse health effects, including cardiomyopathy, thyroid toxicity, blindness, deafness and neurotoxicity [40,41]. Animal studies showed that a portion of Co is retained in tissues for several years [15].…”

Section: Resultsmentioning

confidence: 99%

Role of direct reactivity with metals in chemoprotection by N-acetylcysteine against chromium(VI), cadmium(II), and cobalt(II)

Łuczak

Zhitkovich

2013

Free Radical Biology and Medicine

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The antioxidant N-acetylcysteine (NAC) is widely used for the assessment of the role of reactive oxygen species (ROS) in various biological processes and adverse drug reactions. NAC has been found to effectively inhibit toxicity of carcinogenic metals, which was attributed to its potent ROS-suppressive properties. However, the absence of redox activity among some metals and findings from genetic models suggested a more diverse, smaller role of oxidative stress in metal toxicity. Here, we examined mechanisms of chemoprotection by NAC against Cd(II), Co(II) and Cr(VI) in human cells. We found that NAC displayed a broad-spectrum chemoprotective activity against all three metals, including suppression of cytotoxicity, apoptosis, p53 activation and HSP72 and HIF-1α upregulation. Cytoprotection by NAC was independent of cellular glutathione. NAC strongly inhibited uptake of all three metals in histologically different types of human cells, explaining its high chemoprotective potential. A loss of Cr(VI) accumulation by cells was caused by NAC-mediated extracellular reduction of chromate to membrane-impermeable Cr(III). Suppression of Co(II) uptake resulted from a rapid formation of Co(II)-NAC conjugates that were unable to enter cells. Our results demonstrate that NAC acts through more than one mechanism in preventing metal toxicity and its chemoprotective activity can be completely ROS-independent. A good clinical safety and effectiveness in Co(II) sequestration suggest that NAC could be useful for prevention of tissue accumulation and toxic effects of Co ions released by cobalt-chromium hip prostheses.

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Section: Resultsmentioning

confidence: 99%

Role of direct reactivity with metals in chemoprotection by N-acetylcysteine against chromium(VI), cadmium(II), and cobalt(II)

Łuczak

Zhitkovich

2013

Free Radical Biology and Medicine

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“…To our knowledge no study has yet specifically researched cobalt uptake in neurons and astrocytes. The few in vitro published examples have quantified cobalt accumulation in fibroblast (Sabbioni et al, 2014), bone (Shah et al, 2015) and red blood cells (Simonsen et al, 2011), revealing some interesting findings in the context of cellular cobalt toxicity. For example, cobalt irreversibly accumulates through calcium channels in red blood cells (Simonsen et al, 2011), and osteoblast influx partially traverses through a P2X7R-dependent transporter, while osteoclast cobalt uptake likely relies on endocytosis (Shah et al, 2015).…”

Section: Discussionmentioning

confidence: 99%

“…The few in vitro published examples have quantified cobalt accumulation in fibroblast (Sabbioni et al, 2014), bone (Shah et al, 2015) and red blood cells (Simonsen et al, 2011), revealing some interesting findings in the context of cellular cobalt toxicity. For example, cobalt irreversibly accumulates through calcium channels in red blood cells (Simonsen et al, 2011), and osteoblast influx partially traverses through a P2X7R-dependent transporter, while osteoclast cobalt uptake likely relies on endocytosis (Shah et al, 2015). Moreover, a cobalt-labelling technique has been in use for years to study calcium-permeable AMPA receptors in neurons and certain TRP channels (Aurousseau et al, 2012).…”

Section: Discussionmentioning

confidence: 99%

Cytotoxicity of cobalt chloride in brain cell lines - a comparison between astrocytoma and neuroblastoma cells

Gómez-Arnaiz

Tate

Grant

2020

Toxicology in Vitro

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High levels of circulating cobalt ions in blood have been reported to induce systemic reactions in patients with metal-on-metal (MoM) hip implants. We still lack information regarding these adverse effects, which may specifically impact on patients showing adverse neurological symptoms. To investigate this, we used a battery of in vitro viability and proliferation assays to identify toxic cobalt chloride (CoCl2) concentrations in two different brain cell types: SH-SY5Y neuroblastoma and U-373 astrocytoma cells.Cobalt cytotoxicity was characterised by MTT and Neutral Red (NR) assays at concentrations ranging from 0 to 500M after 24, 48, and 72h exposure. MTT and NR showed a dose-and time-dependent toxicity with cobalt decreasing cell viability at high concentrations. IC50s for MTT at 72h (astrocytes: 333.1522.88; neurons: 100.015.91M) and for BrdU proliferation assays (astrocytes: 212.899.84; neurons: 88.8619.03M) demonstrate that SH-SY5Y neurons are significantly more vulnerable to cobalt than astrocytes. Increased BrdU and MTT assay sensitivity suggested that DNA synthesis and metabolism disruption were involved in Co toxicity.Intracellular cobalt level measured by ICP-MS was significant after 100M treatment.Astrocytes displayed improved resistance to cobalt toxicity and higher uptake, which may reflect their neuroprotective nature. In summary, exposure to high concentrations of extracellular cobalt has deleterious effects in neurons and astrocytes, with neurons showing particular sensitivity.

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“…16 The uptake of all complexes except [Co(tfacen)(NH 3 ) 2 ] + was greater than that of free Co 2+ , administered in the form of Co(NO 3 ) 2 , which enters cells through both ion transporters and by transferrin-mediated pathways. 90,91 To determine whether cobalt uptake correlated with the lipophilicity or cytotoxicity of the complexes, the HPLC retention factors of all complexes were measured using an isocratic mobile phase. Large retention factors correlate with high lipophilicity.…”

Section: Cobalt Uptakementioning

confidence: 99%

Physical properties, ligand substitution reactions, and biological activity of Co(iii)-Schiff base complexes

et al. 2019

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Passive transport pathways for Ca2+ and Co2+ in human red blood cells. 57Co2+ as a tracer for Ca2+ influx

Cited by 12 publications

References 53 publications

Role of direct reactivity with metals in chemoprotection by N-acetylcysteine against chromium(VI), cadmium(II), and cobalt(II)

Role of direct reactivity with metals in chemoprotection by N-acetylcysteine against chromium(VI), cadmium(II), and cobalt(II)

Cytotoxicity of cobalt chloride in brain cell lines - a comparison between astrocytoma and neuroblastoma cells

Physical properties, ligand substitution reactions, and biological activity of Co(iii)-Schiff base complexes

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