Molybdenum, despite its low concentration in the environment, is a critically important element for Earth's
biosphere due to its presence in the most common
nitrogenases. Without molybdenum,
nitrogen fixation would be greatly reduced, and a large part of
biosynthesis as we know it would not occur. Molybdenum is also essential to many individual organisms as a component of enzymes, particularly as part of the
molybdopterin class of
cofactors.
Mo-containing enzymes Molybdenum cofactor.svg|
Molybdopterin complexed with a molybdenum(VI) atom.|alt=Skeletal structure of a molybdopterin with a single molybdenum atom bound to both of the thiolate groups FeMoco cluster.svg|Structure of the
FeMoco active site of
nitrogenase Molybdenum is an essential element in most organisms; a 2008 research paper speculated that a scarcity of molybdenum in the Earth's early oceans may have strongly influenced the evolution of
eukaryotic life (which includes all plants and animals). At least 50 molybdenum-containing enzymes have been identified, mostly in bacteria. Those enzymes include
aldehyde oxidase,
sulfite oxidase and
xanthine oxidase. In terms of function, molybdoenzymes catalyze the oxidation and sometimes reduction of certain small molecules in the process of regulating
nitrogen,
sulfur, and
carbon. In some animals, and in humans, the oxidation of
xanthine to
uric acid, a process of
purine catabolism, is catalyzed by
xanthine oxidase, a molybdenum-containing enzyme. The activity of xanthine oxidase is directly proportional to the amount of molybdenum in the body. An extremely high concentration of molybdenum reverses the trend and can inhibit purine catabolism and other processes. Molybdenum concentration also affects
protein synthesis,
metabolism, and growth. Nitrogenases catalyze the production of ammonia from atmospheric nitrogen: : \mathrm{N_2 + 8 \ H^+ + 8 \ e^- + 16 \ ATP + 16 \ H_2O \longrightarrow 2 \ NH_3 + H_2 + 16 \ ADP + 16 \ P_i} The
biosynthesis of the
FeMoco active site is highly complex. Molybdate is transported in the body as MoO42−.
Human metabolism and deficiency Molybdenum is an essential trace
dietary element. Four mammalian Mo-dependent enzymes are known, all of them harboring a
pterin-based
molybdenum cofactor (Moco) in their active site:
sulfite oxidase,
xanthine oxidoreductase,
aldehyde oxidase, and
mitochondrial amidoxime reductase. People severely deficient in molybdenum have poorly functioning sulfite oxidase and are prone to toxic reactions to sulfites in foods. The human body contains about 0.07 mg of molybdenum per kilogram of body weight, with higher concentrations in the liver and kidneys and lower in the vertebrae. Acute toxicity has not been seen in humans, and the toxicity depends strongly on the chemical state. Studies on rats show a
median lethal dose (LD50) as low as 180 mg/kg for some Mo compounds. Although human toxicity data is unavailable, animal studies have shown that chronic ingestion of more than 10 mg/day of molybdenum can cause diarrhea, growth retardation,
infertility, low birth weight, and
gout; it can also affect the lungs, kidneys, and liver.
Sodium tungstate is a
competitive inhibitor of molybdenum. Dietary tungsten reduces the concentration of molybdenum in tissues. Compared to the United States, which has a greater supply of molybdenum in the soil, people living in those areas have about 16 times greater risk for
esophageal squamous cell carcinoma. Molybdenum deficiency has also been reported as a consequence of non-molybdenum supplemented
total parenteral nutrition (complete intravenous feeding) for long periods of time. It results in high blood levels of
sulfite and
urate, in much the same way as
molybdenum cofactor deficiency. Since pure molybdenum deficiency from this cause occurs primarily in adults, the neurological consequences are not as marked as in cases of congenital cofactor deficiency. A congenital
molybdenum cofactor deficiency disease, seen in infants, is an inability to synthesize
molybdenum cofactor, the heterocyclic molecule discussed above that binds molybdenum at the active site in all known human enzymes that use molybdenum. The resulting deficiency results in high levels of
sulfite and
urate, and neurological damage.
Excretion Most molybdenum is excreted from the human body as molybdate in the urine. Furthermore, urinary excretion of molybdenum increases as dietary molybdenum intake increases. Small amounts of molybdenum are excreted from the body in the feces by way of the bile; small amounts also can be lost in sweat and in hair.
Excess and copper antagonism High levels of molybdenum can interfere with the body's uptake of
copper, producing
copper deficiency. Molybdenum prevents plasma proteins from binding to copper, and it also increases the amount of copper that is excreted in
urine.
Ruminants that consume high levels of molybdenum suffer from
diarrhea, stunted growth,
anemia, and
achromotrichia (loss of fur pigment). These symptoms can be alleviated by copper supplements, either dietary and injection. The effective copper deficiency can be aggravated by excess
sulfur. Copper reduction or deficiency can also be deliberately induced for therapeutic purposes by the compound
ammonium tetrathiomolybdate, in which the bright red anion
tetrathiomolybdate is the copper-chelating agent. Tetrathiomolybdate was first used therapeutically in the treatment of
copper toxicosis in animals. It was then introduced as a treatment in
Wilson's disease, a hereditary copper metabolism disorder in humans; it acts both by competing with copper absorption in the bowel and by increasing excretion. It has also been found to have an inhibitory effect on
angiogenesis, potentially by inhibiting the membrane translocation process that is dependent on copper ions. This is a promising avenue for investigation of treatments for
cancer,
age-related macular degeneration, and other diseases that involve a pathologic proliferation of blood vessels. In some grazing livestock, most strongly in cattle, molybdenum excess in the soil of pasturage can produce scours (
diarrhea) if the pH of the soil is neutral to alkaline; see
teartness.
Mammography Molybdenum targets are used in mammography because they produce X-rays in the energy range of 17-20 keV, which is optimal for imaging soft tissues like the breast. The characteristic X-rays emitted from molybdenum provide high contrast between different types of tissues, allowing for the effective visualization of microcalcifications and other subtle abnormalities in breast tissue. This energy range also minimizes radiation dose while maximizing image quality, making molybdenum targets particularly suitable for breast cancer screening. ==Dietary recommendations==