Effects of dietary zinc deficiency and malnutrition on the T-lymphocyte zinc-finger protein p56[1]c[superscript]k[superscript] in mice
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Date
1997-05-01T00:00:00Z
Authors
Lepage, Lynne Marie Gisele
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Abstract
The objective of this experiment was to investigate the effects of dietary zinc deficiency (ZnDF) and malnutrition syndromes (2% protein deficiency (LP), combined Zn and 2% protein deficiencies (ZnDF + LP) and energy restriction (ER)) compared to the control group (C), on the type of malnutrition, zinc status, splenocyte counts and T-Lymphocyte expression of p56$\rm \sp{lck}$, an early T-lymphocyte signal transduction Zn-finger protein. An adult murine model of zinc deficiency and malnutrition syndromes was developed in order to investigate these parameters. Following a 4 wk feeding trial, mice receiving the ZnDF + LP, ZnDF, ER, and LP diets weighed significantly less than the C group, however, different forms of malnutrition were induced. Protein-type malnutrition was induced in the ZnDF + LP and LP groups, and energy-type malnutrition was induced in the ZnDF and ER groups. Significant decreases in serum zinc and femur zinc pools were observed in the ZnDF + LP and ZnDF groups. A reduction in splenocyte counts was observed in the ZnDF groups. $(1.56 \pm 0.06 \times 10\sp8)$ compared to the C group $(1.91 \pm 0.13 \times 10\sp8),$ however, the ER group $(1.44 \pm 0.03 \times 10\sp8)$ experienced a decrease similar to that of the ZnDF group. The expression of p56$\rm\sp{lck}$ was elevated in all treatment groups compared with the control group. Surprisingly, the ZnDF + LP and the ZnDF groups had approximately a 1.7 fold increase in p56$\sp{\rm lck}$ expression compared to the control group. Thus, it appears that dietary Zn deficiency may play a role in up-regulating the expression of p56$\rm\sp{lck}.$ (Abstract shortened by UMI.)