A variety of inflammatory gastrointestinal diseases are associated with altered zinc metabolism or deficiency. Acute and chronic diarrheal disorders may cause deficiency because of increased losses, altered immunity or decreased absorption. When the small intestinal barrier is altered by inflammation, zinc supplementation may be beneficial not only in correcting the deficiency but also because it improves the small bowel mucosal capacity of absorbing water and electrolytes. Zinc is known to have antioxidant properties being a membrane stabilizer, scavenging reactive oxygen metabolites and regulating cytokine synthesis through the activation of transcription factors and this has relevant potential in inflammatory bowel diseases. Moreover, the element stimulates tissue healing and repair in experimental ulcers directly through promoting cell proliferation, protein synthesis and growth factors production and scavenging free radicals. Interest is growing in supplementary therapies with elements and vitamins but current research suggests great caution and to balance the benefits and dangers of uncontrolled administration, since zinc can also stimulate an increased acute phase response and this can exacerbate chronic relapsing diseases. Zinc plays an important role in inflammation. The metal has catalytic, co-catalytic and structural functions in many zinc-dependent enzymes of the body through the regulation of gene expression. Moreover, the involvement of zinc finger proteins in the genetic expression of growth factors has been established. Zinc stabilizes cellular membranes especially interacting at the SH levels and preventing depolarization of phospholipids. The effects on cellular immunity and especially on the activity of serum thymulin and natural killer cells, T-lymphocyte proliferation and interleukin-2 production are also well-known. A growing body of evidence suggests a role for zinc in antioxidant defence systems. The metal has only one stable oxidation state (divalent) and is not affected by free radicals or oxidative stress. It may act as a scavenger of radical products through the synthesis of enzymes such as superoxide dismutase (SOD) and metallothionein (MT) or it may affect cytokine-activated transcription factors. (C) 2000 Wiley-Liss, Inc.
|Number of pages||7|
|Journal||Journal of Trace Elements in Experimental Medicine|
|Publication status||Published - 2000|
- Gastric diseases
- Inflammatory bowel disease
- Intestinal permeability
ASJC Scopus subject areas