Besides the noble physical appearance of gold and silver, their novel chemical properties attracted the modern technology for various industrial, chemical and biological uses including medical applications. The widespread use of gold and silver, however, can cause potential hazards to our environment. Therefore, suitable detection methods are a prerequisite for the evaluation of their harmful effects as well as for studying their beneficial biological properties. Due to the several advantages over the conventional analytical methods, the fluorescence detection of gold and silver has become an active research area in recent years. In this review, we provide an overview of the reported fluorescent detection systems for gold and silver species, and discuss their sensing properties with promising features. The future scope of developments in this field of research is also mentioned.
A rhodamine-derived alkyne shows turn-on fluorescence change only toward Au(I)/Au(III) species among various other metal species examined. A formyloxazole compound is formed as the major product in aqueous media, presumably via a vinylgold intermediate, which casts new mechanistic implications on vinylgold intermediates.
Zinc performs diverse physiological functions, and virtually all living organisms require zinc as an essential trace element. To identify the detailed function of zinc in fungal pathogenicity, we carried out cDNA microarray analysis using the model system of Aspergillus fumigatus, a fungal pathogen. From microarray analysis, we found that the genes involved in gliotoxin biosynthesis were upregulated when zinc was depleted, and the microarray data were confirmed by northern blot analysis. In particular, zinc deficiency upregulated the expression of GliZ, which encodes a Zn2-Cys6 binuclear transcription factor that regulates the expression of the genes required for gliotoxin biosynthesis. The production of gliotoxin was decreased in a manner inversely proportional to the zinc concentration, and the same result was investigated in the absence of ZafA, which is a zinc-dependent transcription activator. Interestingly, we found two conserved ZafA-binding motifs, 5′-CAAGGT-3′, in the upstream region of GliZ on the genome and discovered that deletion of the ZafA-binding motifs resulted in loss of ZafA-binding activity; gliotoxin production was decreased dramatically, as demonstrated with a GliZ deletion mutant. Furthermore, mutation of the ZafA-binding motifs resulted in an increase in the conidial killing activity of human macrophage and neutrophil cells, and virulence was decreased in a murine model. Finally, transcriptomic analysis revealed that the expression of ZafA and GliZ was upregulated during phagocytosis by macrophages. Taken together, these results suggest that zinc plays an important role in the pathogenicity of A. fumigatus by regulating gliotoxin production during the phagocytosis pathway to overcome the host defense system.
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