Specialized cells, such as the developing oocyte, exhibit unique transition metal signatures and can undergo significant metal uptake and reorganization steps in concert with the specialized function. These patterns of metal utilization are perturbed in the earliest stage of mammalian developmental states, in infectious and neurological diseases, and cancer cell proliferation. While most of these intracellular metal ions are bound tightly in a variety of well characterized metalloenzyme active sites, recent studies of the emerging class of metal trafficking proteins reveal new types of biological coordination chemistry and are opening new questions about how specialized and aberrant cells acquire, deploy, and store these metal ions. Recently, we demonstrated that zinc influx and efflux controls meiotic progression in mammalian oocytes.1 We have shown that total zinc levels in mouse oocytes undergo dramatic fluxes during oocyte maturation, increasing by over 50% in the 12 hour period between GV and MII. Limiting intracellular zinc availability during in vitro maturation using pharmacological means causes formation of large polar bodies and arrest at telophase-I. Intriguingly, when immature oocytes are exposed to low levels of toxic metals such as cadmium and mercury, the developing cell concentrates these metals. A variety of single cell analyticalmethods including STEM-EDS/EELS, X-ray fluorescence microscopy and new fluorescent zinc-specific probes, allow for a comparison between the subcellular distribution of both total zinc and chelator-accessible zinc pools and thus provide insights into intracellular speciation.1Kim AM, Vogt S, O'Halloran TV, Woodruff TK. Zinc availability regulates exit from meiosis in maturing mammalian oocytes. Nat Chem Bio. 2010  Sep;6(9):674-81.

Environmental heavy metal contamination effects on reproductive health: Does essential metal uptake by mammalian oocytes alter development and fertilization?

246th National Meeting (2013)

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