ZINC

Historical aspects
- recognized as a distinct element in 1509
- essentiality in plants in 1869 & animals in 1934
- deficiency syndrome in humans in 1956
Biochemistry
- Atomic number of 30 & an atomic weight of 65,37
- Used by a great number of enzymes & proteins.
- Usually binds to proteins via residues of cysteine &
histidine. Sometimes bound to residues of glutamate or
aspartate. Sometimes plays a catalytic role & some-
times a structural role
Food sources
- Differ widely in their Zn content. Concentration range
from 0,02 mg/ 100 g for egg white, to 1 mg/100 g for
chicken meat and to 75 mg/ 100 g for oysters.
- Shellfish, beef & other red meats are good Zn sources
- Whole-grain cereals are relatively rich in total Zn but
nearly 80% is lost in the wheat milling process.
- Plant Zn concentrations may be enhanced if grown in
Zn-rich soil or treated with Zn-rich fertilizers.
- Animal products provide 70% of the Zn consumed by
people in US, with about half coming from meat.
- Zn intakes are correlated with protein intake, but the
exact relationship is influenced with protein source.
Absorption, Metabolism & Excretion
- Relatively poor. Of the approximately 4 – 14 mg/d
consumed, only 10 – 40% is absorbed.
- Small-molecular-weight ligands, such as amino acids
can increase solubility & facilitate absorption
- large-molecular-weight compounds, such as phytic acid
, form poorly soluble compounds & reduce absorption
- competition between Zn & other elements for binding
sites on the mucosal cell can influence absorbability.
- Cysteine & methionine enhance Zn absorbability by
forming stable complexes with Zn.
- Whole-grain cereal products & plant proteins, such as
soy protein, contain Zn in a less available form.
- The phytic acid (myoinositol hexaphosphate) content of
plant foods explains the lower availability of Zn from
these foods. Fermentation reduces the phytic acid
content & significantly improves Zn absorption.
- The extent of absorption of dietary Zn is relatively high
(50%) when low levels of Zn (5,5 mg/d) are consumed.
The absorption decreases to 25% when higher levels of
Zn (16,5 mg/d) are consumed.
- Large quantities of ingested Zn can interfere with Cu
bioavailability. High intake of Zn induces synthesis of
Cu-binding ligand MT in the mucosal cell.
- Fe given as a supplement or in a liquid solution inhibits
Zn absorption.
- Fe & Zn compete at the same site for for uptake into
mucosal cells.
- High level of dietary Ca impair Zn absorption in
animals, whether this occurs in humans is uncertain.
- Zn is present in all organs, tissues, fluids & secretions
of the body. Zn is primarilly an intracellular ion. Zn is
associated with all organelles of the cell, but 60-80% of
the cellular Zn is found in the cytosol.
- Zn is absorbed all along the small intestine.
- During the process of digesting a meal, digestive
enzymes release dietary Zn from food matrices &
endogenous Zn. Histidine, methionine, cysteine are the
preferred AA ligands.
- Plasma Zn concentration have inverse relationship with
fractional Zn absorption.
- Zn uptake across the brush border surface occurs by
both a carrier-mediated mechanism & a nonmediated
(nonsaturable) component.
- The carrier mechanism predominates at low-normal
luminal concentration of Zn, presumably due to a rise in
the number of receptor sites.
- High Zn intakes, nonsaturable mechanism becomes
prominent. This mechanism may involve passive
diffusion. (figure 1)
- Zn exists in only one valence state: Zn 2+. The normal
70 kg human absorbs 1 to 2 mg/d (figure 2)
Figure 2. Zn balance in normal adults humans
- About 0,05 mmol (3 mg) of Zn is normally circulating
in the plasma. This Zn is partitioned among -2-
macroglobulin (40%), albumin (57%) and AA (3%).
- There is no specific Zn “store”. High Zn intakes
increase bone, liver & intestinal Zn.
- Release of Zn from those tissues during depletion may
slow the rate of onset of Zn deficiency symptoms.
- Reduced food intake associated with Zn deficiency
causes catabolism of muscle tissue & release of Zn into
the plasma.
- Zn excretion occurs primarily via the feces originating
from nonabsorbed Zn, from pancreatic secretions,
mucosal secretions & exfoliated enterocytes.
- Little Zn normally is excreted in urine. Urinary Zn is
300 – 700 g/d, which is equivalent to 2 – 5% of Zn
intake. The onset of dietary Zn deficiency induces a
decline in urinary Zn.
- Plasma Zn levels tend to be maintained during a dietary
deficiency in Zn & decline at a lesser rate than urinary
zinc levels.
- Sweat losses may average about 600 g/d with a high-
zinc diet (34 mg/d) & 200 g/d with a low-Zn diet (4,0
mg/d).
High-Risk Clinical Situations
- Pregnancy  requirement for Zn increase
- Poor maternal Zn status may also cause intrauterine
growth retardation
- Suppl. Zn from midpregnancy to term increased birth
weight & head circumference above that of infants born
to mother receiving placebo
- Zn suppl. is only effective among populations with rela-
tively low plasma Zn concentrations early in pregnancy
- Women with Zn intake in the lowest quartile (<6 mg/d)
had about a 2 X increase in the risk of preterm delivery
- Poor Zn status also associated with increased maternal
morbidity including preeclampsia.
- Several factors may increase the risk of Zn deficiency
in the elderly: reduced capacity to absorb Zn, use of
drugs that increase urinary Zn excretion & consumption
fiber, Ca or Fe suppl. that may alter Zn bioavailability.
- Diseases of the GI tract are frequently complicated by
Zn deficiency  reduces normal absorption of Zn
- Suppl. Zn reduces the duration of acute severe diarrhea,
affect the incidence & duration of diarrheal disorders.
- Altered Zn metabolism occurs in both diabetic humans
& experimental animals.
- Diabetic patients often exhibit hypozincemia & hyper-
zincuria, which increases with the severity of diabetes.
- The mechanisms have not been firmly identified.