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10.1186/s12989-019-0319-z http://scihub22266oqcxt.onion/10.1186/s12989-019-0319-z 31533843!6751682!31533843     free     free     free Deprecated: Implicit conversion from float 235.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 235.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 235.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 235.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 235.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Part+Fibre+Toxicol 2019 ; 16 (1): 35 Nephropedia Template TP {{tp|p=31533843|t=2019. HIF-1alpha is a key mediator of the lung inflammatory potential of lithium-ion battery particles |pdf=|usr=}}{{31533843}} gab.com Text HIF-1alpha is a key mediator of the lung inflammatory potential of lithium-ion battery particles JO: Part Fibre Toxicol http://www.kidney.de/pget.php?&tw=1&pmid=31533843 #FOAvip BACKGROUND: Li-ion batteries (LIB) are increasingly used worldwide. They are made of low solubility micrometric particles, implying a potential for inhalation toxicity in occupational settings and possibly for consumers. LiCoO(2) (LCO), one of the most used cathode material, induces inflammatory and fibrotic lung responses in mice. LCO also stabilizes hypoxia-inducible factor (HIF) -1alpha, a factor implicated in inflammation, fibrosis and carcinogenicity. Here, we investigated the role of cobalt, nickel and HIF-1alpha as determinants of toxicity, and evaluated their predictive value for the lung toxicity of LIB particles in in vitro assays. RESULTS: By testing a set of 5 selected LIB particles (LCO, LiNiMnCoO(2), LiNiCoAlO(2)) with different cobalt and nickel contents, we found a positive correlation between their in vivo lung inflammatory activity, and (i) Co and Ni particle content and their bioaccessibility and (ii) the stabilization of HIF-1alpha in the lung. Inhibition of HIF-1alpha with chetomin or PX-478 blunted the lung inflammatory response to LCO in mice. In IL-1beta deficient mice, HIF-1alpha was the upstream signal of the inflammatory lung response to LCO. In vitro, the level of HIF-1alpha stabilization induced by LIB particles in BEAS-2B cells correlated with the intensity of lung inflammation induced by the same particles in vivo. CONCLUSIONS: We conclude that HIF-1alpha, stabilized in lung cells by released Co and Ni ions, is a mechanism-based biomarker of lung inflammatory responses induced by LIB particles containing Co/Ni. Documenting the Co/Ni content of LIB particles, their bioaccessibility and their capacity to stabilize HIF-1alpha in vitro can be used to predict the lung inflammatory potential of LIB particles. Twit Text FOAVip HIF-1alpha is a key mediator of the lung inflammatory potential of lithium-ion battery particles ????Part Fibre Toxicol http://www.kidney.de/pget.php?&tw=1&pmid=31533843 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=31533843 #FOAvip English Wikipedia <ref>{{Cite pmid|31533843}}</ref> HIF-1alpha is a key mediator of the lung inflammatory potential of lithium-ion battery particles #MMPMID31533843 Sironval V; Palmai-Pallag M; Vanbever R; Huaux F; Mejia J; Lucas S; Lison D; van den Brule S Part Fibre Toxicol 2019[Sep]; 16 (1): 35 PMID31533843show ga BACKGROUND: Li-ion batteries (LIB) are increasingly used worldwide. They are made of low solubility micrometric particles, implying a potential for inhalation toxicity in occupational settings and possibly for consumers. LiCoO(2) (LCO), one of the most used cathode material, induces inflammatory and fibrotic lung responses in mice. LCO also stabilizes hypoxia-inducible factor (HIF) -1alpha, a factor implicated in inflammation, fibrosis and carcinogenicity. Here, we investigated the role of cobalt, nickel and HIF-1alpha as determinants of toxicity, and evaluated their predictive value for the lung toxicity of LIB particles in in vitro assays. RESULTS: By testing a set of 5 selected LIB particles (LCO, LiNiMnCoO(2), LiNiCoAlO(2)) with different cobalt and nickel contents, we found a positive correlation between their in vivo lung inflammatory activity, and (i) Co and Ni particle content and their bioaccessibility and (ii) the stabilization of HIF-1alpha in the lung. Inhibition of HIF-1alpha with chetomin or PX-478 blunted the lung inflammatory response to LCO in mice. In IL-1beta deficient mice, HIF-1alpha was the upstream signal of the inflammatory lung response to LCO. In vitro, the level of HIF-1alpha stabilization induced by LIB particles in BEAS-2B cells correlated with the intensity of lung inflammation induced by the same particles in vivo. CONCLUSIONS: We conclude that HIF-1alpha, stabilized in lung cells by released Co and Ni ions, is a mechanism-based biomarker of lung inflammatory responses induced by LIB particles containing Co/Ni. Documenting the Co/Ni content of LIB particles, their bioaccessibility and their capacity to stabilize HIF-1alpha in vitro can be used to predict the lung inflammatory potential of LIB particles. |Animals[MESH] |Bronchoalveolar Lavage Fluid/chemistry/immunology[MESH] |Cell Culture Techniques[MESH] |Cell Line[MESH] |Cobalt/*toxicity[MESH] |Cytokines/analysis[MESH] |Dose-Response Relationship, Drug[MESH] |Epithelial Cells/*drug effects/metabolism/pathology[MESH] |Female[MESH] |Humans[MESH] |Hypoxia-Inducible Factor 1, alpha Subunit/*metabolism[MESH] |Inhalation Exposure[MESH] |Ions[MESH] |Lung/*drug effects/immunology/pathology[MESH] |Mice[MESH] |Mice, Inbred C57BL[MESH] |Oxides/*toxicity[MESH] |Particle Size[MESH]HIF-1alpha is a key mediator of the lung inflammatory potential of lit(epmc).pdf DeepDyve Pubget Overpricing