Zinc status alters growth and oxidative stress responses in rat hepatoma cells.

Zinc deficiency and excess influence cellular homeostasis and are believed to modulate apoptosis. Zinc also regulates cell growth and proliferation. Understanding of the role of zinc in the mechanisms associated with these changes is limited because of its diverse, complex, and cell-specific effects.

Zinc and cancer: implications for LIV-1 in breast cancer.

Zinc is a trace mineral which is vital for the functioning of numerous cellular processes, is critical for growth, and may play an important role in cancer etiology and outcome. The intracellular levels of this mineral are regulated through the coordinated expression of zinc transporters, which modulate both zinc influx as well as efflux. LIV-1 (ZIP6) was first described in 1988 as an estrogen regulated gene with later work suggesting a role for this transporter in cancer growth and metastasis.

The effects of transformation and ZnT-1 silencing on zinc homeostasis in cultured cells.

We have previously demonstrated that reducing the availability of zinc with the extracellular chelator diethylenetriaminepentaacetic acid (DTPA) promotes efflux of (65)Zn from rat primary hepatocytes and pituitary cells, but increases retention of label in rat hepatoma (H4IIE) and anterior pituitary tumor (GH3) cell lines. To further understand this differential response between primary cells and the corresponding cancer cell lines, we investigated the effects of immortalizing primary cells on their zinc homeostasis. Rat primary hepatocytes were electroporated with the SV40 large T-antigen-coding plasmid pSV3-neo and selected for neomycin resistance.

Rapid homeostatic response of H4IIE cells to diethylenetriaminepentaacetic acid is not due to changes in the amount or localization of ZnT-1 protein.

We have demonstrated that reducing zinc availability with the extracellular chelator diethylenetriaminepentaacetic acid (DTPA) causes rapid inhibition of cellular zinc efflux in H4IIE hepatoma cells but increases zinc efflux in primary hepatocytes. Similar differences were also observed between the rat anterior pituitary cell line GH3 and primary anterior pituitary cells. We hypothesized that the difference between the transformed and primary cells is due to differential regulation of ZnT-1 or SLC-30A-1 because this is the only zinc efflux transporter localized to the plasma membrane.

Acute energy deprivation affects skeletal muscle protein synthesis and associated intracellular signaling proteins in physically active adults.

To date, few studies have characterized the influence of energy deprivation on direct measures of skeletal muscle protein turnover. In this investigation, we characterized the effect of an acute, moderate energy deficit (10 d) on mixed muscle fractional synthetic rate (FSR) and associated intracellular signaling proteins in physically active adults. Eight men and 4 women participated in a 20-d, 2-phase diet intervention study: weight maintenance (WM) and energy deficient (ED; approximately 80% of estimated energy requirements).