An interdisciplinary approach to investigate the impact of cobalt in a human keratinocyte cell line

Bresson, Carole; Lamouroux, C.; Sandre, Caroline; Tabarant, Michel; Gault, Nathalie; Poncy, Jean-Luc; Lefaix, Jean-Louis; Auwer, C. Den; Spezia, Riccardo; Gaigeot, Marie Pierre; Ansoborlo, É.; Mounicou, Sandra; Fraysse, Aurélien; Devès, Guillaume; Bacquart, Thomas; Seznec, Hervé; Pouthier, T.; Moretto, Philippe; Ortega, Richard; Łobiński, Ryszard; Moulin, Christophe

doi:10.1016/j.biochi.2006.09.003

Cited by 18 publications

(21 citation statements)

References 46 publications

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“…The intra‐cellular localization of Co 2+ to nuclear and perinuclear sites in osteoblasts is consistent with its known interactions with genomic DNA and nuclear proteins associated with DNA repair . Our finding that Co 2+ was also distributed throughout the cell body is in keeping with the distribution of other divalent cations, such as Ca 2+ and Zn 2+ that have established plasma membrane channels and transporters, and may suggest use of similar transport machinery.…”

Section: Discussionsupporting

confidence: 82%

Understanding the tissue effects of tribo‐corrosion: Uptake, distribution, and speciation of cobalt and chromium in human bone cells

Shah

Quinn

Gartland

et al. 2014

Journal Orthopaedic Research

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Cobalt and chromium species are released in the local tissues as a result of tribo-corrosion, and affect bone cell survival and function. However we have little understanding of the mechanisms of cellular entry, intracellular distribution, and speciation of the metals that result in impaired bone health. Here we used synchrotron based X-ray fluorescence (XRF), X-ray absorption spectroscopy (XAS), and fluorescent-probing approaches of candidate receptors P2X7R and divalent metal transporter-1 (DMT-1), to better understand the entry, intra-cellular distribution and speciation of cobalt (Co) and chromium (Cr) in human osteoblasts and primary human osteoclasts. We found that both Co and Cr were most highly localized at nuclear and perinuclear sites in osteoblasts, suggesting uptake through cell membrane transporters, and supported by a finding that P2X7 receptor blockade reduced cellular entry of Co. In contrast, metal species were present at discrete sites corresponding to the basolateral membrane in osteoclasts, suggesting cell entry by endocytosis and trafficking through a functional secretory domain. An intracellular reduction of Cr 6þ to Cr 3þ was the only redox change observed in cells treated with Co 2-4We, and others, have previously shown that these concentrations of Co and Cr affect bone cell survival and function in-vitro, 5-7 and associate with systemically measurable effects on bone mass and bone turnover in patients. 8 In order to understand the adverse effects of metal debris exposure on bone health and how these effects may be mitigated, it is necessary to understand how metal enters the relevant cell populations, and their intracellular distribution and speciation characteristics. In this study we have used microfocus X-ray spectroscopy, an analytical technique that uses highenergy X-ray beams derived by synchrotron radiation, to determine the chemical form and oxidation state of an element in microscopic samples.9-11 Specifically, we have used Microfocus X-ray fluorescence (m-XRF) to measure the elemental distribution and micro-X-ray absorption near-edge structure (m-XANES) to characterize the chemical form of the metals in human bone cells.We also investigated the role of two candidate metal transporters, the P2X7 receptor (P2X7R) and the divalent metal transport-1 (DMT-1), in the cellular entry of Co and Cr in human bone cells. The P2X7R is expressed in both human osteoblasts and osteoclasts and plays an important role in bone homeostasis. 12,13The DMT-1 is a ubiquitously expressed transporter of ferrous iron and a broad range of other divalent cations, including Co 2þ

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Section: Discussionsupporting

confidence: 82%

Understanding the tissue effects of tribo‐corrosion: Uptake, distribution, and speciation of cobalt and chromium in human bone cells

Shah

Quinn

Gartland

et al. 2014

Journal Orthopaedic Research

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“…To directly assess Co-induced toxicity, the distribution and biochemical speciation of Co in human keratinocytes (HaCaT) exposed to Co(II) was studied by a combination of PIXE and RBS 437. Keratinocytes are responsible for maintaining the architecture of the epidermis.…”

Section: Microprobe X-ray Fluorescence Imaging Techniquesmentioning

confidence: 99%

“…The ion beam data showed that exposure to excess Co(II) resulted in a dose-dependent accumulation of Co(II) predominantly within the cytosol. Areas with high Co and Fe levels were observed in the extracellular space, presumably caused from precipitation of sparingly soluble sphaerocobaltite (CoHCO 3 ) 437. Prompted by suggestions that Co-induced toxicity involves interference with DNA repair mechanisms,439 Ortega et al performed PIXE as well as SXRF analysis in tomography mode at the single cell level to elucidate the three-dimensional distribution of Co 440.…”

Section: Microprobe X-ray Fluorescence Imaging Techniquesmentioning

confidence: 99%

In Situ Imaging of Metals in Cells and Tissues

et al. 2009

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“…In nuclear plants, it can occur in two radioactive forms of cobalt, 58 Co and 60 Co, which are formed from corrosion-erosion of alloys containing cobalt and other metals. These two forms produce high-energy γ photons, which can be used in radiotherapy to fight tumours [ 5 , 6 ].…”

Section: Introductionmentioning

confidence: 99%

Review paper Selected aspects of the action of cobalt ions in the human body

Czarnek¹,

Terpiłowska²,

Siwicki³

2015

cejoi

156

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Cobalt is widespread in the natural environment and can be formed as an effect of anthropogenic activity. This element is used in numerous industrial applications and nuclear power plants. Cobalt is an essential trace element for the human body and can occur in organic and inorganic forms. The organic form is a necessary component of vitamin B12 and plays a very important role in forming amino acids and some proteins in nerve cells, and in creating neurotransmitters that are indispensable for correct functioning of the organism. Its excess or deficiency will influence it unfavourably. Salts of cobalt have been applied in medicine in the treatment of anaemia, as well as in sport as an attractive alternative to traditional blood doping. Inorganic forms of cobalt present in ion form, are toxic to the human body, and the longer they are stored in the body, the more changes they cause in cells. Cobalt gets into the body in several ways: firstly, with food; secondly by the respiratory system; thirdly, by the skin; and finally, as a component of biomaterials. Cobalt and its alloys are fundamental components in orthopaedic implants and have been used for about 40 years. The corrosion of metal is the main problem in the construction of implants. These released metal ions may cause type IV inflammatory and hypersensitivity reactions, and alternations in bone modelling that lead to aseptic loosening and implant failure. The ions of cobalt released from the surface of the implant are absorbed by present macrophages, which are involved in many of the processes associated with phagocytose orthopaedic biomaterials particles and release pro-inflammatory mediators such as interleukin-1 (IL-1), interleukin-6 (IL-6), tumour necrosis factor α (TNF-α), and prostaglandin.

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An interdisciplinary approach to investigate the impact of cobalt in a human keratinocyte cell line

Cited by 18 publications

References 46 publications

Understanding the tissue effects of tribo‐corrosion: Uptake, distribution, and speciation of cobalt and chromium in human bone cells

Understanding the tissue effects of tribo‐corrosion: Uptake, distribution, and speciation of cobalt and chromium in human bone cells

In Situ Imaging of Metals in Cells and Tissues

Review paper Selected aspects of the action of cobalt ions in the human body

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