The essentiality of
zinc for humans was recognized only 40 years ago.
Zinc deficiency was suspected to occur in Iranian patients with growth retardation,
hypogonadism in males, hepato-
splenomegaly, rough and dry skin,
geophagia and severe
iron deficiency anemia. Later we documented
zinc deficiency in similar patients in Egypt. The diet of these patients consisted of mainly cereal
proteins which contained high
phytate and this led to decreased availability of
iron and
zinc. These patients had severe immune dysfunctions, inasmuch as they died of intercurrent
infections by the time they were 25 years of age. In our studies in experimental human model of
zinc deficiency, we documented decreased serum
testosterone level,
oligospermia, severe immune dysfunctions mainly affecting T helper cells, decreased serum
thymulin activity
hyperammonemia, neuro-
sensory disorders and decreased lean body mass. The basic mechanisms of
zinc action on immune cells have been reviewed in this paper. Our studies showed that the activation of many
zinc dependent
enzymes and
transcription factors were affected adversely due to
zinc deficiency. The gene expression and production of Th1
cytokines were affected adversely due to
zinc deficiency.
Zinc is also an
antioxidant and has anti-inflammatory actions. We have reported decreased plasma
zinc, increased plasma oxidative stress markers and increased generation of inflammatory
cytokines in the elderly subjects which were corrected by
zinc supplementation. In cell culture studies, we have observed that
zinc induces A20 which inhibits
NF-kappaB activation resulting in decreased generation of inflammatory
cytokines.