Background:

Zinc Pyrithione is an antifungal and antibacterial agent disrupting membrane transport by blocking the proton pump.Target: Proton PumpZinc pyrithione is considered as a coordination complex of zinc. The pyrithione ligands, which are formally monoanions, are chelated to Zn 2+ via oxygen and sulfur centers. In the crystalline state, zinc pyrithione exists as a centrosymmetric dimer, where each zinc is bonded to two sulfur and three oxygen centers. In solution, however, the dimers dissociate via scission of one Zn-O bond. Zinc pyrithione, which is a dimer but is probably biologically active as a monomer, induces plasma membrane depolarization with half-maximal effect (K1/2) of about 0.3 mM [1]. Zinc pyrithione is an unusual synthetic potentiator that potently activates both heterologous and native M channels by inducing channel opening at the resting potential [2]. Zinc pyrithione rapidly accumulated in the tissues of the exposed mussels, proportionately to both exposure concentration and time. Even though the 7-d median lethal concentration (LC50) = 8.27 μM established here appears high with respect to reported ZnPT environmental concentrations, the results indicate that this biocide could represent a threat for marine organisms in coastal environments and that further investigations on its biological effects at sublethal doses are needed [3].

参考文献:
[1]. Ermolayeva, E. and D. Sanders, Mechanism of pyrithione-induced membrane depolarization in Neurospora crassa. Appl Environ Microbiol, 1995. 61(9): p. 3385-90.
[2]. Xiong, Q., H. Sun, and M. Li, Zinc pyrithione-mediated activation of voltage-gated KCNQ potassium channels rescues epileptogenic mutants. Nat Chem Biol, 2007. 3(5): p. 287-96.
[3]. Marcheselli, M., C. Rustichelli, and M. Mauri, Novel antifouling agent zinc pyrithione: determination, acute toxicity, and bioaccumulation in marine mussels (Mytilus galloprovincialis). Environ Toxicol Chem, 2010. 29(11): p. 2583-92.