| Zinc (Zn) is an essential trace mineral attributed with several biological activities working via mineral-protein and mineral-DNA interactions. Mammals have developed a highly organized and well balanced system that responds to changes in Zn bioavailability. In the presence of a low Zn environment, Zn influx and efflux transporters are altered to increase Zn transport into the cells, and decrease the amount of Zn released. Zn transport has been shown to be important in the developing embryo at different stages; the redundancy in the multiple isoforms of Zn transporters may provide a protective mechanism such that Zn import and export are not mediated by one transporter. The work described in this dissertation examines the effects of low Zn on; (1) heart formation in rat embryos, and (2) the role of Zn transporters in the regulation of osteoblast cells. The results show that Zn deficiency has deleterious effects on cardiac neural crest cells metabolism leading to abnormal heart formation. In addition, data is presented showing that osteoblast cells actively express various Zn transporters, and the expression of the transporters is altered in the face of Zn deficiency. The underlying pathways involved in Zn-deficiency associated heart and bone cellular abnormalities remain to be fully defined. The current data show that Zn is required for significant biological functions and that a deficiency of Zn can lead to abnormal heart and skeletal tissue development. |
