Metabolism and Excretion

Knowledge about chemical changes that must occur before excretion for most of the ultratrace elements is quite limited. Perhaps the best characterized is inorganic arsenic, which is methylated into monomethylarsonic acid and dimethylarsinic acid, and organic arsenic, which is converted into, or remains mostly as, arsenobetaine before being excreted in the urine. Other ultratrace elements that are known to be incorporated into biochemical metabolites for transport and/or excretion include aluminum bound to transferrin, cadmium incorporated into metallo-thionein, nickel as the a-2-macroglobulin nickeloplasmin or bound to albumin and L-histidine, and vanadium converted into vanadyl-transferrin and vanadyl-ferritin (see Table 1). A known important metabolite of molybdenum is a small nonprotein cofactor containing a pterin nucleus that is present at the active site of molybdoenzymes. More than 40% of molybdenum not attached to an enzyme in liver also exists as this cofactor bound to the mitochondrial outer membrane. This form can be transferred to an apoenzyme of xanthine oxidase or sulfite oxidase, which transforms it into an active enzyme molecule. Molecules of biological importance for the ultratrace elements are shown in Table 2. The ultratrace elements are excreted from the body mainly via the feces and urine. Fecal excretion of absorbed ultratrace elements

Table 1 Absorption, transport, and storage characteristics of the ultratrace elements

Element Major machanism(s)

for homeostasis

Means of absorption

Percentage of ingested absorbed

Transport and storage vehicles

Aluminum

Absorption

Arsenic

Boron

Bromine

Cadmium

Fluorine

Germanium

Urinary excretion: Inorganic arsenic as mostly dimethylarsinic acid and organic arsenic as mostly arsenobetaine

Urinary excretion

Urinary excretion

Absorption

50% daily intake excreted in urine; about 50% daily intake stored in bone and developing teeth

Urinary excretion

Uncertain; some evidence far passive diffusion through the paracellular pathway; also, evidence for active absorption through processes shared with active processes of calcium; probably occurs in proximal duodenum; citrate combined with aluminum enhances absorption Inorganic arsenate becomes sequestered in or on mucosal tissue, then absorption involves a simple movement down a concentration gradient; organic arsenic absorbed mainly by simple diffusion through lipid regions of the intestinal boundary Ingested boron is converted into B(OH)3 and absorbed in this form, probably by passive diffusion Probably passive diffusion because no apparent saturable component May share a common absorption mechanism with other metals (e.g., zinc) but mechanism is less efficient for cadmium Absorption by passive diffusion and inversely related to pH. Significant portion absorbed as hydrogen fluoride from stomach; absorption of fluoride also occurs throughout the small intestine Has not been conclusively determined but most likely is by passive diffusion

Less than 1%

Soluble inorganic forms, >90%; slightly soluble inorganic forms, 20-30%; inorganic forms with foods, 60-75%; methylated forms, 45-90%

Greater than 90%

Greater than 90%

Transferrin carries aluminum in plasma; bone a possible storage site

Before excretion inorganic arsenic is converted into monomethyl arsonic acid and dimethylarsinic acid; arsenobetaine not biotransformed; arsenocholine transformed to arsenobetaine

Boron transported through the body as undissociated B(OH)3; bone a possible storage site None identified

Incorporated into metallothionein, which probably is both a storage and transport vehicle

Exists as fluoride ion in plasma; hydrogen fluoride is the form in diffusion equilibration across cell membranes. Stored in bone

None identified

Table 1 Continued

Element

Major machanism(s)

Means of absorption

Percentage of ingested

Transport and storage

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