Biological effects of Ni(II) on monocytes and macrophages in normal and hyperglycemic environments

Chana, Monica; Lewis, Jill B.; Davis, Ryan R.; Elam, Yolanda; Hobbs, D.T.; Lockwood, Petra E.; Wataha, John C.; Messer, Regina L. W.

doi:10.1002/jbm.a.36437

Cited by 6 publications

(5 citation statements)

References 37 publications

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“…The analysis of cell number and cellular activity revealed the impact of metal ions on metabolic activity by showing a significant decrease in activity that was mainly prominent in 500 μM cobalt-and nickel ion-treated cells. Similar results for nickel ions were reported by Chana et al [13]. The loss of metabolic activity was accompanied by a massive release of reactive oxygen species.…”

Section: Discussionsupporting

confidence: 89%

“…As found by us (data not shown) and also reported by Lund et al [12], THP-1 derived macrophages de-differentiate, detach from the surface of the cell culture dish and show a round monocyte-like morphology after more than 48 h without PMA. However, the simultaneous presence of PMA in THP-1 macrophage culture was shown to interfere with the effects of nickel ions [13]. We therefore decided to differentiate for 24 h with PMA, to then remove PMA from the cell culture and to limit the incubation time with metal ions to 48 h.…”

Section: Cell Culturementioning

confidence: 99%

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Comparison of Inflammatory Effects in THP-1 Monocytes and Macrophages after Exposure to Metal Ions

et al. 2020

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Monocytes and macrophages are the first barrier of the innate immune system, which interact with abrasion and corrosion products, leading to the release of proinflammatory mediators and free reactive molecules. The aim of this study was to understand inflammation-relevant changes in monocytes and macrophages after exposure to corrosion products. To do this, the THP-1 cell line was used to analyze the effects of metal ions simultaneously in monocytes and differentiated macrophages. Cells were stimulated with several concentrations of metal salts (CoCl2, NiCl2, CrCl3 × 6H2O) to analyze viability, gene expression, protein release and ROS production. Untreated cells served as negative controls. While exposure to Cr(3+) did not influence cell viability in both cell types, the highest concentration (500 µM) of Co(2+) and Ni(2+) showed cytotoxic effects mirrored by significantly reduced metabolism, cell number and a concomitant increase of ROS. The release of IL-1β, IL-8, MCP-1 and M-CSF proteins was mainly affected in macrophages after metal ion exposure (100 µM), indicating a higher impact on pro-inflammatory activity. Our results prove that monocytes and macrophages react very sensitively to corrosion products. High concentrations of bivalent ions lead to cell death, while lower concentrations trigger the release of inflammatory mediators, mainly in macrophages.

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Section: Discussionsupporting

confidence: 89%

Section: Cell Culturementioning

confidence: 99%

Comparison of Inflammatory Effects in THP-1 Monocytes and Macrophages after Exposure to Metal Ions

et al. 2020

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“…The higher prevalence of nickel allergy in obese individuals (Lusi et al, 2015) was associated with a worse metabolic profile, while reducing the oral intake of nickel led to a considerable reduction in the BMI (Lusi et al, 2015;Watanabe et al, 2018). Chana et al (2018) confirmed that nickel (II) amplifies LPS-induced secretion of several pro-inflammatory cytokines from monocytes. It is known that hyperglycaemic conditions also affect monocytic function.…”

Section: Immunotoxic Activity Of Nickelmentioning

confidence: 69%

“…Chana et al. (2018) confirmed that nickel (II) amplifies LPS‐induced secretion of several pro‐inflammatory cytokines from monocytes. It is known that hyperglycaemic conditions also affect monocytic function.…”

Section: Assessmentmentioning

confidence: 95%

Update of the risk assessment of nickel in food and drinking water

Schrenk¹,

Bignami²,

Bodin³

et al. 2020

EFS2

101

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The European Commission asked EFSA to update its previous Opinion on nickel in food and drinking water, taking into account new occurrence data, the updated benchmark dose (BMD) Guidance and newly available scientific information. More than 47,000 analytical results on the occurrence of nickel were used for calculating chronic and acute dietary exposure. An increased incidence of postimplantation loss in rats was identified as the critical effect for the risk characterisation of chronic oral exposure and a BMDL 10 of 1.3 mg Ni/kg body weight (bw) per day was selected as the reference point for the establishment of a tolerable daily intake (TDI) of 13 lg/kg bw. Eczematous flare-up reactions in the skin elicited in nickel-sensitised humans, a condition known as systemic contact dermatitis, was identified as the critical effect for the risk characterisation of acute oral exposure. A BMDL could not be derived, and therefore, the lowest-observed-adverse-effect-level of 4.3 lg Ni/kg bw was selected as the reference point. The margin of exposure (MOE) approach was applied and an MOE of 30 or higher was considered as being indicative of a low health concern. The mean lower bound (LB)/upper bound (UB) chronic dietary exposure was below or at the level of the TDI. The 95th percentile LB/UB chronic dietary exposure was below the TDI in adolescents and in all adult age groups, but generally exceeded the TDI in toddlers and in other children, as well as in infants in some surveys. This may raise a health concern in these young age groups. The MOE values for the mean UB acute dietary exposure and for the 95th percentile UB raises a health concern for nickel-sensitised individuals. The MOE values for an acute scenario regarding consumption of a glass of water on an empty stomach do not raise a health concern.

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“…Ni 2+ also activates the expression of intercellular adhesion molecules on endothelial cells and keratinocytes, therefore amplifying the inflammatory response [66]. More recently, Ni 2+ and particularly NiSO 4 has been shown to alter inflammatory cytokine secretion from monocytes [67] by modulating transcription factor signaling pathways such as the nuclear factor kappa B (NF-kB), that regulate cytokine secretion [68, 69]. However, Ni 2+ does not alter the activation or nuclear translocation efficiency of NF-kB [70]; emerging evidence suggest that redox status generated by Ni 2+ regulates the nuclear activity of NF-kB proteins [71] by altering the binding of NF-kB proteins to DNA [70].…”

Section: Discussionmentioning

confidence: 99%

Nuclear factor erythroid 2 – related factor 2 and its relationship with cellular response in nickel exposure: a systems biology analysis

Jiménez-Vidal

Espitia-Pérez

Torres-Ávila

et al. 2019

BMC Pharmacol Toxicol

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BackgroundNickel and nickel-containing compounds (NCC) are known human carcinogens. However, the precise molecular mechanisms of nickel-induced malignant transformation remain unknown. Proposed mechanisms suggest that nickel and NCC may participate in the dual activation/inactivation of enzymatic pathways involved in cell defenses against oxidative damage, where Nuclear factor-erythroid 2 related factor 2 (Nrf2) plays a central role.MethodsFor assessing the potential role of proteins involved in the Nrf2-mediated response to nickel and NCC exposure, we designed an interactome network using the STITCH search engine version 5.0 and the STRING software 10.0. The major NCC-protein interactome (NCPI) generated was analyzed using the MCODE plugin, version 1.5.1 for the detection of interaction modules or subnetworks. Main centralities of the NCPI were determined with the CentiScape 2.2 plugin of Cytoscape 3.4.0 and main biological processes associated with each cluster were assessed using the BiNGO plugin of Cytoscape 3.4.0.ResultsWater-soluble NiSO4 and insoluble Ni3S2 were the most connected to proteins involved in the NCPI network. Nfr2 was detected as one of the most relevant proteins in the network, participating in several multifunctional protein complexes in clusters 1, 2, 3 and 5. Ontological analysis of cluster 3 revealed several processes related to unfolded protein response (UPR) and response to endoplasmic reticulum (ER) stress.ConclusionsCellular response to NCC exposure was very comparable, particularly concerning oxidative stress response, inflammation, cell cycle/proliferation, and apoptosis. In this cellular response, Nfr2 was highly centralized and participated in several multifunctional protein complexes, including several related to ER-stress. These results add evidence on the possible Ni2+ induced – ER stress mainly associated with insoluble NCC. In this scenario, we also show how protein degradation mediated by ubiquitination seems to play key roles in cellular responses to Ni.

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Biological effects of Ni(II) on monocytes and macrophages in normal and hyperglycemic environments

Cited by 6 publications

References 37 publications

Comparison of Inflammatory Effects in THP-1 Monocytes and Macrophages after Exposure to Metal Ions

Comparison of Inflammatory Effects in THP-1 Monocytes and Macrophages after Exposure to Metal Ions

Update of the risk assessment of nickel in food and drinking water

Nuclear factor erythroid 2 – related factor 2 and its relationship with cellular response in nickel exposure: a systems biology analysis

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