PubMed Health⌕ Search

PubMed · 10163513

Trace elements in pediatrics.

Abstract

This review discusses biologic roles, metabolism, and clinical aspects of three essential trace elements, zinc, copper, and selenium. Clinical situations that result in disturbed trace element metabolism, and signs or symptoms that may suggest a trace element problem are listed. Important issues for trace element assay development are emphasized, and examples of pediatric reference ranges provided.

Explore related subjects

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

G Lockitch. 1996. Trace elements in pediatrics.. https://pubmed.ncbi.nlm.nih.gov/10163513/

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related citations

Copper-Containing Surface Engineering for Soft-Tissue Biomedical Devices: Structure-Function Relationships and Ion Release-Driven Biological Performance, A Systematic Review.

Copper and copper-based materials have gained increasing attention for the functional modification of implantable medical devices intended for prolonged soft-tissue contact, including vascular stents, catheters, and intrauterine devices. Owing to their broad-spectrum antimicrobial activity, redox reactivity, and involvement in angiogenesis and cellular signaling, copper-based systems offer significant potential for multifunctional surface engineering. However, achieving a balance between antibacterial efficacy, corrosion behavior, controlled ion release, and cytocompatibility remains a critical challenge. This PRISMA-compliant systematic review analyzes copper-containing materials and surface modification strategies for soft-tissue biomedical applications. A structured search of Scopus, Web of Science, and PubMed (2015-2025) identified 65 eligible studies. The review encompasses bulk copper-containing alloys, electrochemical and chemical surface modification techniques, physical vapor deposition approaches, and advanced hybrid systems integrating copper with polymers, hydrogels, or metal-phenolic networks. Across the reviewed literature, antibacterial performance was strongly dependent on copper concentration, microstructural distribution, and spatiotemporal ion release profiles. Moderate, well-controlled copper incorporation frequently improved antibacterial efficacy while maintaining acceptable hemocompatibility and cytocompatibility, particularly in vascular and blood-contacting devices. In contrast, excessive copper loading often accelerated corrosion and induced adverse cellular responses. Emerging multifunctional architectures demonstrated improved regulation of biological interactions, enabling simultaneous antibacterial, antithrombotic, and proendothelial effects. Overall, copper-based surface technologies represent a versatile platform for soft-tissue implant modification. Future translational progress will require precise control of copper release kinetics and comprehensive long-term in vivo validation to ensure safety and sustained therapeutic performance. From the authors' perspective, the most promising future direction involves multifunctional copper-based hybrid coatings capable of dynamically regulating ion release, host tissue integration, and antibacterial performance simultaneously. Strategies integrating hierarchical architectures, stimulus-responsive release systems, and clinically scalable fabrication methods are expected to play a key role in translating copper-containing surfaces from experimental concepts toward commercially viable soft-tissue biomedical devices.

Copper↗

Inhibition of oxygen evolution in Photosystem II by Cu(II) ions is associated with oxidation of cytochrome b559.

We have found that elevated copper concentrations, apart from the inhibition of oxygen evolution, changed the initial states distribution of the oxygen-evolving complex. Already at low concentrations, copper ions oxidized the low-potential form of cytochrome b (559) and also its high-potential form at higher concentrations at which fluorescence quenching was observed. We suggest that the primary target sites in Photosystem II for copper is tyrosine(z), both cytochrome b (559) forms and chlorophyll(z), and that these sites are the source of the copper-induced fluorescence quenching and oxygen evolution inhibition in Photosystem II.

Copper↗

Altered Cu metabolism and differential transcription of Cu/ZnSod genes in a Cu/ZnSOD-deficient mutant of maize: evidence for a Cu-responsive transcription factor.

Maize inbred line A351 exhibits extremely low levels of Cu/Zn superoxide dismutase (SOD) isozymes, three cytosolic and one chloroplastic, which are increased by supplying copper to near-toxic concentrations. Activities of the copper enzymes cytochrome c oxidase and ascorbate oxidase are also reduced. The level of expression of the maize copper chaperone for SOD is normal to elevated. The gene transcript encoding chloroplastic SOD-1 is present at normal levels, whereas RNA levels of the cytosolic SODs are low and increase with added copper, suggesting a promoter element and copper-dependent transcription factor common to the three genes. Although a reduced level of high-affinity copper transport in A351 cannot be ruled out, high transcript levels of a constitutively expressed metallothionein, suggesting increased copper chelation capacity and creating a general copper-deprivation effect, seem to be a likely cause of the reduced levels of copper enzyme activity and Cu/ZnSod gene transcripts. While exogenous copper does not affect the wild-type SOD activity or protein, it increases wild-type Cu/ZnSod transcript levels in a response similar to that of several yeast genes involved in copper sequestration and antioxidant defense. A sequence that is highly homologous to those of the copper-responsive transcription factors ACE1 (Saccharomyces cerevisiae) and AMT1 (Candida glabrata) is present in the promoters of three maize Cu/ZnSod genes.

Copper↗