ArticlePloS one2017
Regulatory effects of zinc on cadmium-induced cytotoxicity in chronic inflammation.
Article in PloS one, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers, 1 of them a synthesis that pooled it.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
10 citing papers in PubMed, 1 synthesis or guideline pooled it, 19 citations in OpenAlex.
- Update on Tenosynovial Giant Cell Tumor, an Inflammatory Arthritis With Neoplastic Features.Frontiers in immunology · 2022Pooled it
- Zinc Sulfate Alleviates Olanzapine Induced Alteration in Hepatic Protein Patterns and Antioxidant Defense System in Rats.Biological trace element research · 2026Article
- HLA-B27 may modulate the interaction between ERAP1 polymorphisms and smoking in ankylosing spondylitis patients.Molecular biology reports · 2022Article
- Use of Generalized Weighted Quantile Sum Regressions of Tumor Necrosis Factor Alpha and Kidney Function to Explore Joint Effects of Multiple Metals in Blood.International journal of environmental research and public health · 2022Article
- Synoviocytes from pigmented villonodular synovitis are less sensitive to cadmium-induced cell death than synoviocytes from rheumatoid arthritis.Scientific reports · 2022Article
- Bioactive phytochemicals from Salvia officinalis attenuate cadmium-induced oxidative damage and genotoxicity in rats.Environmental science and pollution research international · 2021Article
- Importance of lymphocyte-stromal cell interactions in autoimmune and inflammatory rheumatic diseases.Nature reviews. Rheumatology · 2021Review
- Zinc as a countermeasure for cadmium toxicity.Acta pharmacologica Sinica · 2021Review
- The Impact of a Polyphenol-Rich Extract from the Berries ofNutrients · 2020Article
- A Sensitive, Nonradioactive Assay for Zn(II) Uptake into Metazoan Cells.Biochemistry · 2018Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectivesZinc (Zn) has major effects on immune system activation while Cadmium (Cd) has anti-inflammatory and anti-proliferative effects in several chronic inflammatory contexts. The aim of this work was to investigate by which mechanisms Zn could compete with Cd and eventually counteract its deleterious effects. Rheumatoid arthritis (RA) synoviocytes exposed to cytokines were used as a model of chronic inflammation; osteoarthritis (OA) synoviocytes were used as control.
methodsCell/medium fractionation constants were analyzed for different metals by inductively-coupled-plasma mass-spectrometry by comparison to the 70Zn spike. Interleukin-17 (IL-17) and tumor necrosis factor-alpha (TNF-α) were used to mimic inflammation. Gene expression of ZIP-8 importer, metallothioneins-1 (MT-1s) and the ratio between metalloprotease-3 and the tissue inhibitor of metalloproteinases (MMP-3)/TIMP-1) were evaluated after pre-exposure to cytokines and Cd, with or without the addition of exogenous Zn (0.9 ppm). Cell viability was measured by neutral red assay and IL-6 production by ELISA.
resultsSynoviocytes selectively absorbed and retained Cd in comparison to Zn. Metal import increased with IL-17/TNF-α exposure, through the enhanced ZIP-8 expression. Zn did not modify ZIP-8 expression, while Cd reduced it (p<0.05). Zn induced a reduction of Cd-induced MT-1s expression, in particular of MT-1X (3-fold), and subsequently the final intra-cellular content of Cd. By reducing Cd accumulation in cells, Zn reversed Cd anti-proliferative and anti-inflammatory effects but preserved the low MMP-3/TIMP-1 ratio induced by Cd, which was enhanced by inflammatory conditions.
conclusionZinc counteracts the deleterious effect of Cd by reducing its import and accumulation in the cell, without the reactivation of destructive pathways such as MMPs.
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