Nickel, cobalt and chromium-induced cytotoxicity and intracellular accumulation in human hacat keratinocytes

Ermolli, Monica; Menné, Charlotte; Pozzi, Giovanni; Serra, Miquel Àngel; Clerici, Libero

doi:10.1016/s0300-483x(00)00373-5

Cited by 80 publications

(49 citation statements)

References 29 publications

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“…In agreement with the previous study (Ermolli et al, 2001), exposure of HaCaT cells to CoCl 2 dose-dependently attenuated cell viability. Interestingly, we found that treatment of HaCaT cells with CoCl 2 enhanced generation of ROS and oversecretion of both IL-6 and IL-8, which was not reported by Ermolli and his coworkers (Ermolli et al, 2001).…”

Section: Discussionsupporting

confidence: 93%

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Oxidative Stress Mediates Chemical Hypoxia-Induced Injury and Inflammation by Activating NF-κb-COX-2 Pathway in HaCaT Cells

Liu

Ling

Mei-fen

et al. 2011

Molecules and Cells

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Hypoxia of skin is an important physiopathological process in many diseases, such as pressure ulcer, diabetic ulcer, and varicose ulcer. Although cellular injury and inflammation have been involved in hypoxia-induced dermatic injury, the underlying mechanisms remain largely unknown. This study was conducted to investigate the effects of cobalt chloride (CoCl 2 ), a hypoxia-mimicking agent, on human skin keratinocytes (HaCaT cells) and to explore the possible molecular mechanisms. Exposure of HaCaT cells to CoCl 2 reduced cell viability and caused overproduction of reactive oxygen species (ROS) and oversecretion of interleukin-6 (IL-6) and interleukin-8 (IL-8). Importantly, CoCl 2 exposure elicited overexpression of cyclooxygenase-2 (COX-2) and phosphorylation of nuclear factor-kappa B (NF-κB) p65 subunit. Inhibition of COX-2 by NS-398, a selective inhibitor of COX-2, significantly repressed the cytotoxicity, as well as secretion of IL-6 and IL-8 induced by CoCl 2 . Inhibition of NF-κB by PDTC (a selective inhibitor of NF-κB) or genetic silencing of p65 by RNAi (Si-p65), attenuated not only the cytotoxicity and secretion of IL-6 and IL-8, but also overexpression of COX-2 in CoCl 2 -treated HaCaT cells. Neutralizing anti-IL-6 or anti-IL-8 antibody statistically alleviated CoCl 2 -induced cytotoxicity in HaCaT cells. N-acetyl-L-cysteine (NAC), a well characterized ROS scavenger, obviously suppressed CoCl 2 -induced cytotoxicity in HaCaT cells, as well as secretion of IL-6 and IL-8. Additionally, NAC also repressed overexpression of COX-2 and phosphorylation of NF-B κ p65 subunit induced by CoCl 2 in HaCaT cells. In conclusion, our results demonstrated that oxidative stress mediates chemical hypoxia-induced injury and inflammatory response through activation of NF-κB-COX-2 pathway in HaCaT cells.

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Section: Discussionsupporting

confidence: 93%

“…Interestingly, we found that treatment of HaCaT cells with CoCl 2 enhanced generation of ROS and oversecretion of both IL-6 and IL-8, which was not reported by Ermolli and his coworkers (Ermolli et al, 2001). Similarly, CoCl 2 induced overproduction of ROS in PC12 cells (Jung and Kim, 2004;Zou et al, 2001) and H9c2 cells (Chen et al, 2010).…”

Section: Discussioncontrasting

confidence: 44%

Oxidative Stress Mediates Chemical Hypoxia-Induced Injury and Inflammation by Activating NF-κb-COX-2 Pathway in HaCaT Cells

Liu

Ling

Mei-fen

et al. 2011

Molecules and Cells

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“…Contrary, in artificial saliva alone the release of ions from uncoated NiTi decreases with the prolonged time of immersion, because the protective oxide layer remains stable 3,18,19) . The daily dosage of 5 µg of nickel which induce epithelial proliferation 34) , was observed for the NiTi wire during the first three days, and during the third week when using prophylactic agents with high HF concentration. For the NNiTi wire, epithelial proliferation could be expected during the first three days, and during the first three weeks when using prophylactic agents with high HF concentration.…”

Section: Discussionmentioning

confidence: 96%

Effect of pH, fluoride and hydrofluoric acid concentration on ion release from NiTi wires with various coatings

Katić

Ćurković

Bošnjak³

et al. 2017

Dent. Mater. J.

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Aim was to determine effect of pH, fluoride (F − ) and hydrofluoric acid concentration (HF) on dynamic of nickel (Ni 2+ ) and titanium (Ti 4+ ) ions release. Nickel-titanium wires with untreated surface (NiTi), rhodium (RhNiTi) and nitride (NNiTi) coating were immersed once a week for five min in remineralizing agents, followed by immersion to artificial saliva. Ion release was recorded after 3, 7, 14, 21 and 28 days. Pearson correlations and linear regression were used for statistical analysis. Release of Ni 2+ from NiTi and NNiTi wires correlated highly linearly positively with HF (r=0.948 and 0.940, respectively); for RhNiTi the correlation was lower and negative (r=−0.605; p<0.05). The prediction of Ti 4+ release was significant for NiTi (r=0.797) and NNiTi (r=0.788; p<0.05) wire. Association with F − was lower; for pH it was not significant. HF predicts the release of ions from the NiTi wires better than the pH and F − of the prophylactic agents.

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“…This element accumulates in the core structure of microorganism cells. Ermolli et al reported that 0.475 mM Co +2 produced a toxic effect on HaCaT human keratinocytes and that this effect could only be observed after 4 h [23] . It was found in our study however, the lethal effect of Co +2 on E. histolytica was presented at lower concentrations such as 0.05 mM and was increased dose-dependently.…”

Section: +2mentioning

confidence: 99%

Effects of Cd⁺², Cu⁺², Ba⁺²and Co⁺²ions onEntamoeba histolyticacysts

Aksoy¹,

Üstün²,

Dağcı³

et al. 2004

WJG

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AIM:The effects of cobalt, copper, cadmium and barium ions on the cysts of Entamoeba histolytica (E. histolytica), an amebic dysentery agent, cultured in Robinson medium were investigated.METHODS: E. histolytica cysts and trophozoites isolated from a patient with amebiasis were cultivated in the medium, incubated at 37 for a period of 4 days and 40×10 4 /ml amebic cysts were then transferred to a fresh medium. At the second stage, 0.05, 0.1 and 0.2 mM of selected metal ions were added to the medium, and the effects of these ions on parasitic reproduction compared with the control group were observed. RESULTS:It was determined that the number of living parasites in all the groups containing metal ions decreased significantly starting from 30 minutes (P<0.01). CuCl 2 showed the highest lethal effect on E. histolytica cysts, whereas the lowest lethal effect was observed with CoCl 2 . It was also seen that the number of living cells was decreased as the ion concentration and exposure time were increased, and that there were no living parasites in the medium at the end of 24 h (P<0.01). CONCLUSION:It may be stated that the effect of everincreasing contamination of the environment with metal waste materials on parasites should be investigated further.

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Nickel, cobalt and chromium-induced cytotoxicity and intracellular accumulation in human hacat keratinocytes

Cited by 80 publications

References 29 publications

Oxidative Stress Mediates Chemical Hypoxia-Induced Injury and Inflammation by Activating NF-κb-COX-2 Pathway in HaCaT Cells

Oxidative Stress Mediates Chemical Hypoxia-Induced Injury and Inflammation by Activating NF-κb-COX-2 Pathway in HaCaT Cells

Effect of pH, fluoride and hydrofluoric acid concentration on ion release from NiTi wires with various coatings

Effects of Cd⁺², Cu⁺², Ba⁺²and Co⁺²ions onEntamoeba histolyticacysts

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Nickel, cobalt and chromium-induced cytotoxicity and intracellular accumulation in human hacat keratinocytes

Cited by 80 publications

References 29 publications

Oxidative Stress Mediates Chemical Hypoxia-Induced Injury and Inflammation by Activating NF-κb-COX-2 Pathway in HaCaT Cells

Oxidative Stress Mediates Chemical Hypoxia-Induced Injury and Inflammation by Activating NF-κb-COX-2 Pathway in HaCaT Cells

Effect of pH, fluoride and hydrofluoric acid concentration on ion release from NiTi wires with various coatings

Effects of Cd+2, Cu+2, Ba+2and Co+2ions onEntamoeba histolyticacysts

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Effects of Cd⁺², Cu⁺², Ba⁺²and Co⁺²ions onEntamoeba histolyticacysts