Zinc regulates DNA synthesis and IL‐2, IL‐6, and IL‐10 production of PWM‐stimulated PBMC and normalizes the periphere cytokine concentration in chronic liver disease
1997; Wiley; Volume: 10; Issue: 1 Linguagem: Inglês
10.1002/(sici)1520-670x(1997)10
ISSN1520-670X
AutoresDirk Reinhold, S Ansorge, Kurt Grüngreiff,
Tópico(s)Pregnancy and Medication Impact
ResumoZinc (zinc ions and/or chelated zinc) plays an important role in the maintenance of immune function. Patients with chronic liver disease, particularly liver cirrhosis, frequently have endotoxemia, increased serum concentrations of cytokines, e.g., interleukin-6 (IL-6), and reduced serum zinc levels. The aim of the present study was to investigate the effects of zinc (ZnCl2, ZnO, ZnSO4) on DNA synthesis and cytokine production (IL-2, IL-6, IL-10) in pokeweed mitogen (PWM)-stimulated peripheral blood mononuclear cells (PBMC). In addition, we examined the effect of long-term zinc supplementation (zinc-hydrogenaspartate; UNIZINK 50; 3 × 1 = 29.76 mg/day) on IL-6 and IL-10 serum levels in patients with chronic liver disease (n = 16), all with reduced serum zinc levels. It could be shown that zinc concentrations up to 0.1 mM stimulate DNA synthesis and cytokine production by PWM-stimulated PBMC, whereas higher concentrations (0.2–0.4 mM) have a strongly inhibitory effect. Zinc concentrations exceeding 0.5 mM were found to have a toxic effect on these immune cells. Interestingly, in most patients with chronic liver disease (n = 10), zinc supplementation decreased IL-6, and to a lesser extent, IL-10 serum levels, and normalized the serum zinc concentrations. We conclude that zinc plays a regulatory role in DNA synthesis and cytokine production by PBMC. The critical zinc concentration for immune cells lies in the range of 0.5 mM, which is equivalent to a daily dose of ∼45 mg zinc salt. Furthermore, zinc supplementation in chronic liver disease with reduced serum zinc levels appears to normalize IL-6 and IL-10 production. J. Trace Elem. Exp. Med. 10:19–27, 1997. © 1997 Wiley-Liss, Inc.
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