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The development of metallic joint prostheses has been ongoing for more than a century alongside advancements in hip and knee arthroplasty. Among the materials utilized, the Cobalt-Chromium-Molybdenum (Co-Cr-Mo) and Titanium-Aluminum-Vanadium (Ti-Al-V) alloys are predominant in joint prosthesis construction, predominantly due to their commendable biocompatibility, mechanical strength, and corrosion resistance. Nonetheless, over time, the physical wear, electrochemical corrosion, and inflammation induced by these alloys that occur post-implantation can cause the release of various metallic components. The released metals can then flow and metabolize in vivo, subsequently causing potential local or systemic harm. This review first details joint prosthesis development and acknowledges the release of prosthetic metals. Second, we outline the metallic concentration, biodistribution, and elimination pathways of the released prosthetic metals. Lastly, we discuss the possible organ, cellular, critical biomolecules, and significant signaling pathway toxicities and adverse effects that arise from exposure to these metals.

In this study, we elucidate the effect of different sonication techniques to efficiently prepare particle dispersions from selected non-functionalized NPs (Cu, Al, Mn, ZnO), and corresponding consequences on the particle dose, surface charge and release of metals. Probe sonication was shown to be the preferred method for dispersing non-inert, non-functionalized metal NPs (Cu, Mn, Al). However, rapid sedimentation during sonication resulted in differences between the real and the administered doses in the order of 30–80 % when sonicating in 1 and 2.56 g/L NP stock solutions. After sonication, extensive agglomeration of the metal NPs resulted in rapid sedimentation of all particles. DLVO calculations supported these findings, showing the strong van der Waals forces of the metal NPs to result in significant NP agglomeration. Metal release from the metal NPs was slightly increased by increased sonication. The addition of a stabilizing agent (bovine serum albumin) had an accelerating effect on the release of metals in sonicated solutions. For Cu and Mn NPs, the extent of particle dissolution increased from <1.6 to ~5 % after sonication for 15 min. A prolonged sonication time (3–15 min) had negligible effects on the zeta potential of the studied NPs. In all, it is shown that it is of utmost importance to carefully investigate how sonication influences the physico-chemical properties of dispersed metal NPs. This should be considered in nanotoxicology investigations of metal NPs. Graphical Abstract

Understanding the interactions between biomedical alloys and body fluids is of importance for the successful and safe performance of implanted devices. Albumin, as the first protein that comes in contact with an implant surface, can determine the biocompatibility of biomedical alloys. The interaction of albumin with biomedical alloys is a complex process influenced by numerous factors. This literature overview aims at presenting the current understanding of the mechanisms of serum albumin (both Bovine Serum Albumin, BSA, and Human Serum Albumin, HSA) interactions with biomedical alloys, considering only those research works that present a mechanistic description of the involved phenomena. Widely used biomedical alloys, such as 316L steel, CoCrMo and Titanium alloys are specifically addressed in this overview. Considering the literature analysis, four albumin-related phenomena can be distinguished: adsorption, reduction, precipitation, and protein-metal binding. The experimental techniques used to understand and quantify those phenomena are described together with the studied parameters influencing them. The crucial effect of the electrochemical potential on those phenomena is highlighted. The effect of the albumin-related phenomena on corrosion behavior of biomedical materials also is discussed.

Welders are daily exposed to various levels of welding fumes containing several metals. This exposure can lead to an increased risk for different health effects which serves as a driving force to develop new methods that generate less toxic fumes. The aim of this study was to explore the role of released metals for welding particle-induced toxicity and to test the hypothesis that a reduction of Cr(VI) in welding fumes results in less toxicity by comparing the welding fume particles of optimized Cr(VI)-reduced flux-cored wires (FCWs) to standard FCWs. The welding particles were thoroughly characterized, and toxicity (cell viability, DNA damage and inflammation) was assessed following exposure to welding particles as well as their released metal fraction using cultured human bronchial epithelial cells (HBEC-3kt, 5–100 µg/mL) and human monocyte-derived macrophages (THP-1, 10–50 µg/mL). The results showed that all Cr was released as Cr(VI) for welding particles generated using standard FCWs whereas only minor levels (< 3% of total Cr) were released from the newly developed FCWs. Furthermore, the new FCWs were considerably less cytotoxic and did not cause any DNA damage in the doses tested. For the standard FCWs, the Cr(VI) released in cell media seemed to explain a large part of the cytotoxicity and DNA damage. In contrast, all particles caused rather similar inflammatory effects suggesting different underlying mechanisms. Taken together, this study suggests a potential benefit of substituting standard FCWs with Cr(VI)-reduced wires to achieve less toxic welding fumes and thus reduced risks for welders.

Implantation using stainless steels (SS) is an example where an understanding of protein-induced metal release from SS is important when assessing potential toxicological risks. Here, the protein-induced metal release was investigated for austenitic (AISI 304, 310, and 316L), ferritic (AISI 430), and duplex (AISI 2205) grades in a phosphate buffered saline (PBS, pH 7.4) solution containing either bovine serum albumin (BSA) or lysozyme (LSZ). The results show that both BSA and LSZ induce a significant enrichment of chromium in the surface oxide of all stainless steel grades. Both proteins induced an enhanced extent of released iron, chromium, nickel and manganese, very significant in the case of BSA (up to 40-fold increase), whereas both proteins reduced the corrosion resistance of SS, with the reverse situation for iron metal (reduced corrosion rates and reduced metal release in the presence of proteins). A full monolayer coverage is necessary to induce the effects observed.

This paper assesses whether copper surfaces retain their anti‐viral efficacy, or whether this property is altered by exposure to the cleaning solutions of glutaraldehyde or NaClO, when used in high‐touch surfaces that are regularly touched by many people. The results obtained show that copper has a virus titer of 50% after 30 and 60 min of exposure, but for Cu‐30Ni, 50% is not reached until 70 and 80 min in artificial sweat after cleaning. Cu‐30Ni has more effective resistance to tarnishing. Copper and nickel ions are released from Cu and Cu‐30Ni samples in NaClO and glutaraldehyde solutions. A brief exposure to disinfectant solutions causes corrosion product formation on both Cu and Cu‐30Ni surfaces, primarily composed of Cu2O. In contrast, CuO and Cu(OH)2 are the primary compounds that contribute to creating a thicker film formed as exposure time is increased. Phases containing chlorine are present in the corrosion product composition. This research introduces a new understanding of how copper and Cu‐30Ni alloys respond to disinfectant solutions and humid air. The Cu‐30Ni alloy offers superior corrosion resistance, retaining a shiny appearance, but simultaneously reflects an increased viral inactivation time due to a more stable oxide layer compared to pure copper. This study evaluates the antiviral efficacy and corrosion behavior of pure copper and Cu‐30Ni alloy on high‐touch surfaces under simulated public conditions with periodic cleaning. Copper shows faster virus inactivation due to higher ion release, while Cu‐30Ni offers better aesthetic durability. Disinfectant type significantly influences oxide formation, ion release, and antiviral performance.

Gold nanoparticles (AuNPs) have the potential to be used in various biomedical applications, partly due to the inertness and stability of gold. Upon intravenous injection, the NPs interact with the mononuclear phagocyte system, first with monocytes in the blood and then with macrophages in tissue. The NP-macrophage interaction will likely affect the stability of the AuNPs, but this is seldom analyzed. This study aimed to elucidate the role of macrophages in the biodissolution of AuNPs and underlying mechanisms. With an in vitro dissolution assay, we used inductively coupled plasma mass spectrometry to quantitatively compare the dissolution of 5 and 20 nm AuNPs coated with citrate or PEG in cell medium alone or in the presence of THP1-derived macrophages at 24 hours. In addition, we analyzed the cell dose, compared extra- and intracellular dissolution, and explored the possible role of reactive nitrogen species. The results showed a higher cellular dose of the citrate-coated AuNPs, but dissolution was mainly evident for those sized 5 nm, irrespective of coating. The macrophages clearly assisted the dissolution, which was approximately fivefold higher in the presence of macrophages. The dissolution, however, appeared to take place mainly extracellularly. Acellular experiments demonstrated that peroxynitrite can initiate oxidation of gold, but a ligand is required to keep the gold ions in solution. This study suggests extracellular dissolution of AuNPs in the presence of macrophages, likely with the contribution of the release of reactive nitrogen species, and provides new insight into the fate of AuNPs in the body.

Complex metal oxides (CMOs) are used broadly in applications including electroreactive forms found in lithium-ion battery technology. Computational chemistry can provide unique information about how the properties of CMO cathode materials change in response to changes in stoichiometry, for example, changes of the lithium (Li) content during the charge–discharge cycle of the battery. However, this is difficult to measure experimentally due to the small cross-sectional area of the cations. Outside of operational conditions, the Li content can influence the transformations of the CMO when exposed to the environment. For example, metal release from CMOs in aqueous settings has been identified as a cross-cutting mechanism important to CMO degradation. Computational studies investigating metal release from CMOs show that the thermodynamics depend on the oxidation states of lattice cations, which is expected to vary with the lithium content. In this work, computational studies track changes in metal release trends as a function of Li content in Lix(Ni1/3Mn1/3Co1/3)O2 (NMC). The resulting dataset is used to construct a random forest tree (RFT) machine learning (ML) model. A modeling challenge in delithiation studies is the large configurational space to sample. Through investigating multiple configurations at each lithium fraction, we find structural features associated with favorable energies to chemically guide the identification of relevant structures and adequately predict voltage values.

Hydrogenated amorphous carbon (a-C:H) has been considered a promising biocompatible coating to protect metallic alloys against corrosion for medical applications, namely orthodontics. However, there is still no optimal solution for this biomedical field; hence, the investigation remains open. In this work, the effect of a nonmetallic doping element (N) on sputter-deposited a-C:H coatings was studied concerning both salivary corrosion and cytotoxicity behavior. After a 30-day corrosion test in an acidic modified Fusayama-Meyer artificial saliva, metal release from both coated and uncoated 316L stainless steel (SS) substrates was quantified. Tests on the corrosion extracts were then performed by using monocultures of macrophages and fibroblasts, and their coculture; and cell viability was evaluated via the MTT test. Results show an overall inhibition of the SS corrosion, which enhanced the in vitro biocompatibility with a minimal effect on the coatings’ microstructure. Among all the coatings tested, the undoped a-C:H coating performed the best, whereas an increase in N doping led to poorer protection against metal dissolution and a subsequent slightly lower biocompatibility. The findings corroborate that selecting the nonmetallic element N for doping C-based coatings is not a good choice for this biomedical field, even at low contents up to 10 at.%.

Corrosion and metal release mechanisms of the biomedical stainless steel grade Type 316L are at human-relevant biological conditions not fully understood. This study focuses on its corrosion properties and release of iron (Fe), chromium (Cr), manganese (Mn), and nickel (Ni) into simulated physiological solutions at pH 7.4 in the presence of proteins. Parallel studies were performed on stainless steel Type 303 containing a substantial amount of MnS inclusions. Metal release studies were performed in phosphate buffered saline (PBS) for 4 h and 24 h at 37°C with or without different concentrations of bovine serum albumin (BSA), fibrinogen from bovine plasma (Fbn), or mixtures of the same. Studies were in addition performed after 1, 4, 6, and 24 h in solutions that were partially replenished after 5 h in order to investigate whether any Vroman effect (exchange of adsorbed proteins by proteins of higher binding affinity) could influence the extent of released metals in solution. This was performed at physiological concentrations of BSA (40 g/L) and Fbn (2.67 g/L) in PBS, and for reference solutions of PBS, PBS with 40 g/L BSA, and PBS with 2.67 g/L Fbn. Changes in open-circuit potential and linear polarization resistance were investigated for the same conditions. After exposure, the exposed surfaces were rinsed and investigated ex situ by means of x-ray photoelectron spectroscopy and infrared reflection absorption spectroscopy. Metal-protein complexation-induced metal release mechanisms were found to be most pronounced for Type 316L and the release of Fe, Cr, and Ni. Fibrinogen adsorbed differently onto Type 303 (thicker conformation of adsorbed proteins) as compared with Type 316L and occasionally induced corrosion events for Type 303. Mn was mostly released from inclusions present in the Type 303 alloy, most probably via non-electrochemical mechanisms. A Vroman effect was observed for both grades. A significant extent of precipitation of metal-rich protein aggregates influenced the metal release measurements in solution and resulted in an underestimation of the total amount of released metals from the stainless steel grades.