Background: Implantations of metallic biomedical devices into bodies are increasing. The elution of Ni ions from these devices can lead to metal allergies. However, the molecular mechanisms of the elution have not been fully examined. Furthermore, it is not clear whether infection and inflammation affect the corrosion of metals.
Objective: We examined whether the elution of Ni from metal wires and plates was enhanced by inflammation in vivo and in vitro.
Methods: A Ni or SUS316L wire was implanted subcutaneously in the dorsum of mice. Lipopolysaccharide (LPS) was injected at the site immediately following the implantation. After 8, 24, and 72 h, the tissue around the wire was excised. RAW 264 cells were seeded on a Ni plate and incubated for 24h in medium containing LPS. The amount of Ni in the tissue or conditioned medium was determined fluorometrically.
Results: The release of Ni ions from the wire was significantly increased from 8 to 72 h, and further increased by LPS. LPS also enhanced the release of Ni ions by the cells, but only when they were attached to the Ni plate. Chloroquine, bafilomycin A(1) and amiloride markedly inhibited the effects of LPS.
Conclusion: The activation of inflammatory cells on metals enhanced the elution of Ni probably via the release of protons at the interface of the cells and material.
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http://dx.doi.org/10.1016/j.jdermsci.2010.12.006 | DOI Listing |
J Control Release
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Department of Ophthalmology, Changzhou Third Peopls's Hospital, Changzhou Clinical College of Xuzhou Medical University, 300 Lanlin North road, Changzhou, Jiangsu 213000, China. Electronic address:
Neutrophil extracellular traps (NETs) promote neovascularization during the acute phase after ocular chemical injury, while the local inflammatory acidic environment delays post-injury repair. Currently, the mechanism of NETs promoting neovascularization has not been fully elucidated, and there is a lack of therapeutic strategies to effectively improve the local microenvironment for corneal repair. In this study, we validated the NETs-M2-angiogenic pathway after injury.
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Jiangxi Province Key Laboratory of Additive Manufacturing of Implantable Medical Device, Jiangxi University of Science and Technology, Nanchang 330013, China; State Key Laboratory of Precision Manufacturing for Extreme Service Performance, College of Mechanical and Electrical Engineering, Central South University, Changsha 410083, China. Electronic address:
The overexpression of glutathione (GSH) within the tumor microenvironment has long been considered as the major obstacle for reactive oxygen species (ROS)-based antitumor therapies. To address this challenge, a selenite (SeO) and ferric ion co-doped hydroxyapatite (SF-HAP) nanohybrid was synthesized, which is then introduced into poly-L-lactic acid (PLLA) to prepare porous scaffold by selective laser sintering to continuously release Fe and SeO ions. Of great significance is the released SeO catabolize GSH to generate superoxide anion (O) rather than directly eliminating GSH, thereby reversing the obstacle posed by its overexpression and achieving a "waste-to-treasure" transformation.
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January 2025
National Key Laboratory of Space Medicine, China Astronaut Research and Training Center, Beijing 100094, China.
TMEM16A, a key calcium-activated chloride channel, is crucial for many physiological and pathological processes such as cancer, hypertension, and osteoporosis, etc. However, the regulatory mechanism of TMEM16A is poorly understood, limiting the discovery of effective modulators. Here, we unveil an allosteric gating mechanism by presenting a high-resolution cryo-EM structure of TMEM16A in complex with a channel inhibitor that we identified, Tamsulosin, which is resolved at 2.
View Article and Find Full Text PDFJ Biomed Mater Res A
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Department of Biomedical Engineering, Amirkabir University of Technology (Tehran Polytechnic), Tehran, Iran.
In situ gelling, cell-laden hydrogels hold promise for regenerating tissue lesions with irregular shapes located in complex and hard-to-reach anatomical sites. A notable example is the regeneration of neural tissue lost due to cerebral cavitation. However, hypoxia-induced cell necrosis during the vascularization period imposes a significant challenge to the success of this approach.
View Article and Find Full Text PDFSci Rep
December 2024
Department of Chemistry and Biochemistry, Centre for Research in Molecular Modeling (CERMM), Concordia University, 7141 Sherbrooke Street West, Montréal, QC, H4B 1R6, Canada.
Nitroglycerin is a potent vasodilator in clinical use since the late 1800s. It functions as a prodrug that is bioactivated by formation of an enzyme-based thionitrate, E-Cys-NO. This intermediate reportedly decomposes to release NO and NO but their relative yields remain controversial.
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