Quality Control of 2,9-Dimethyl-1,10-phenanthroline hemihydrate. Aromatic heterocyclic compounds can also be classified according to the number of heteroatoms contained in the heterocycle: single heteroatom, two heteroatoms, three heteroatoms and four heteroatoms. Compound: 2,9-Dimethyl-1,10-phenanthroline hemihydrate, is researched, Molecular C28H26N4O, CAS is 34302-69-7, about Exploiting the vulnerable active site of a copper-only superoxide dismutase to disrupt fungal pathogenesis. Author is Robinett, Natalie G.; Culbertson, Edward M.; Peterson, Ryan L.; Sanchez, Hiram; Andes, David R.; Nett, Jeniel E.; Culotta, Valeria C..
Copper-only superoxide dismutases (SODs) represent a new class of SOD enzymes that are exclusively extracellular and unique to fungi and oomycetes. These SODs are essential for virulence of fungal pathogens in pulmonary and disseminated infections, and we show here an addnl. role for copper-only SODs in promoting survival of fungal biofilms. The opportunistic fungal pathogen Candida albicans expresses 3 copper-only SODs, and deletion of 1 of them, SOD5, eradicated candidal biofilms on venous catheters in a rodent model. Fungal copper-only SODs harbor an irregular active site that, unlike their Cu,Zn-SOD counterparts, contains a copper co-factor unusually open to solvent and lacks zinc for stabilizing copper binding, making fungal copper-only SODs highly vulnerable to metal chelators. Unlike mammalian Cu,Zn-SOD1, C. albicans SOD5 indeed rapidly loses its copper to metal chelators such as EDTA, and binding constants for Cu(II) predict that copper-only SOD5 has a much lower affinity for copper than does Cu,Zn-SOD1. We screened compounds with a variety of indications and identified several metal-binding compounds, including the ionophore pyrithione zinc (PZ), that effectively inhibit C. albicans SOD5 but not mammalian Cu,Zn-SOD1. PZ both acts as an ionophore that promotes uptake of toxic metals and inhibits copper-only SODs. The pros and cons of a vulnerable active site for copper-only SODs and the possible exploitation of this vulnerability in antifungal drug design are discussed.
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