Molybdenum metabolism

It is clear that both the form of molybdenum administered and the route of exposure affect molybdenum metabolism and survival (Table 30.4). By comparison, adverse effects (some deaths) were noted at 250 mg Mo/kg body weight (BW) (in guinea pigs), at 50 mg/kg BW in domestic cats (central nervous system impairment), at 10 mg/L drinking water in mice (survival), at 10 to 15 mg total daily intake in humans (high incidence of gout-like disease), and at to 3 mg/m3 air in humans for 5 years (respiratory difficulties), or 6 to 19 mg/m3 in humans for 4 years (Table 30.4). 

Suttle, N.F. and A.C. Field. 1983. Effects of dietary supplements of thiomolybdates on copper and molybdenum metabolism in sheep. Jour Comp. Pathol. 93 379-389. 

Van Ryssen, J.B.J. and W.J. Stielau. 1980. The effect of various levels of dietary copper and molybdenum on copper and molybdenum metabolism in sheep. S. Afr Jour. Anim. Sci. 10 37-47. 

Taylor SR, McLennan SM (1985) The Continental Crust Its Composition and Evolution. Blackwell, Boston Tuit CB, Ravizza G (2003) The marine distribution of molybdenum. Geochim Cosmochim Acta 67 A4950 Tumlund JR, Keyes WR, Peiffer GL (1993) Isotope ratios of molybdenum determined by thermal ionization mass spectrometry for stable isotope studies of molybdenum metabolism in humans. Anal Chem 65 1717-1722... 

Anke M, Kronemann H, Hoeemann G, Grun M and Groppel B (1981) Molybdenum metabolism in ruminants suffering from molybdenum dfidency. Mengen-und Spurenelemente 1 211—216. 

Duran M, Beemee FA, Heiden C, Koeteiand J, DE Beee PK, Brink M and Wadman SK (1978) Combined deficiency ofi xanthine oxidase and sulfite oxidase a defect of molybdenum metabolism of transport J Inher Metab Dis 1 175-178. Eedman JA, Ebens RJ and Case AA (1978) Molyb-denosis a potential problem in ruminants grazing on coal mine spoils. J Range Manage 31 34-36. 

Molybdenum Metabolism and Requirements in Humans Judith R. Turnlund... 

Molybdenum is considered an ultra-trace element with an approximate amount of 5 mg in the adult human body. It is a cofactor for at least three enzymes in humans (sulfite oxidase, xanthine oxidase, and aldehyde oxidase) and is involved in the catabolism of sulfur-containing amino acids, purine, and pyrimidine. A better understanding of human molybdenum metabolism is needed in order to give evidence-based recommendations regarding optimal nutrition, although molybdenum deficiency and associated pathological symptoms have not yet been observed in humans [74]. 

Sievers, E., Domer, K., Garbe-Schonberg, D., and Schaub, J. (2001) Molybdenum metabolism stable isotope studies in infancy, f Trace Elem. Med. Biol., 15, 185-191. 

It appears that chromium(III) is an essential trace element in mammalian metabolism and, together with insulin, is responsible for the clearance of glucose from the blood-stream. Tungsten too has been found to have a role in some enzymes converting CO2 into formic acid but, from the point of view of biological activity, the focus of interest in this group is unquestionably on molybdenum. 

In animal metabolism, oxomolybdoenzymes catalyse a number of oxidation processes. These oxidases contain Mo coordinated to terminal O and S atoms, and their action appears to involve loss of an O or S atom along with reduction to Mo or Mo". It is, however, the role of molybdenum in nitrogen fixation which has received most attention. 

Bauder R, B Tshisuaka, F Lingens (1990) Microbial metabolism of quinoline and related compounds VII. Quinoline oxidoreductase from Pseudomonas putida a molybdenum-containing enzyme. Biol Chem Hoppe-Seyler 371 1137-1144. 

Hdschle B, D Jendrossek (2005) Utilization of geraniol is dependent on molybdenum in Pseudomonas aeruginosa. evidence for different metabolic routes for oxidation of geraniol and citronellol. Microbiology (UK) 151 2277-2283. 

De Beyer A, E Lingens (1993) Microbial metabolism of quinoline and related compounds XVI. Quinaldine oxidoreductase from Arthrobacter spec. Rii 61a a molybdenum-containing enzyme catalysing the hydroxylation at C-4 of the heterocycle. Biol Chem Eloppe-Seyler 374 101-120. 

In the first family, the metal is coordinated by one molecule of the pterin cofactor, while in the second, it is coordinated to two pterin molecules (both in the guanine dinucleotide form, with the two dinucleotides extending from the active site in opposite directions). Some enzymes also contain FejSj clusters (one or more), which do not seem to be directly linked to the Mo centers. The molybdenum hydroxylases invariably possess redox-active sites in addition to the molybdenum center and are found with two basic types of polypeptide architecture. The enzymes metabolizing quinoline-related compounds, and derivatives of nicotinic acid form a separate groups, in which each of the redox active centers are found in separate subunits. Those enzymes possessing flavin subunits are organized as a2jS2A2, with a pair of 2Fe-2S centers in the (3 subunit, the flavin in the (3 subunit, and the molybdenum in the y subunit. 

In summary, we may add that bacterial utilization of quinoline and its derivatives as a rule depends on the availability of traces of molybdate in the culture medium [363], In contrast, growth of the bacterial strains on the first intermediate of each catabolic pathway, namely, the lH-2-oxo or 1 II-4-oxo derivatives of the quinoline compound was not affected by the availability of molybdate. This observation indicated a possible role of the trace element molybdenum in the initial hydroxylation at C2. In enzymes, Mo occurs as part of the redox-active co-factor, and all the Mo-enzymes involved in N-heteroatomic compound metabolism, contain a pterin Mo co-factor. The catalyzed reaction involves the transfer of an oxygen atom to or from a substrate molecule in a two-electron redox reaction. The oxygen is supplied by the aqueous solvent. Certainly, the Mo-enzymes play an important role in the initial steps of N-containing heterocycles degradation. 

Use of the first oxidised products by proto-aerobic organisms - sulfate, ferric ions, and probably nitrogen oxides. Molybdenum became more available and was generally required for N and S metabolism (three to two billion years ago). 

Chromium has proved effective in counteracting the deleterious effects of cadmium in rats and of vanadium in chickens. High mortality rates and testicular atrophy occurred in rats subjected to an intraperitoneal injection of cadmium salts however, pretreatment with chromium ameliorated these effects (Stacey et al. 1983). The Cr-Cd relationship is not simple. In some cases, cadmium is known to suppress adverse effects induced in Chinese hamster (Cricetus spp.) ovary cells by Cr (Shimada et al. 1998). In southwestern Sweden, there was an 80% decline in chromium burdens in liver of the moose (Alces alces) between 1982 and 1992 from 0.21 to 0.07 mg Cr/kg FW (Frank et al. 1994). During this same period in this locale, moose experienced an unknown disease caused by a secondary copper deficiency due to elevated molybdenum levels as well as chromium deficiency and trace element imbalance (Frank et al. 1994). In chickens (Gallus sp.), 10 mg/kg of dietary chromium counteracted adverse effects on albumin metabolism and egg shell quality induced by 10 mg/kg of vanadium salts (Jensen and Maurice 1980). Additional research on the beneficial aspects of chromium in living resources appears warranted, especially where the organism is subjected to complex mixtures containing chromium and other potentially toxic heavy metals. 

Clarification of copper interactions with molybdenum, sulfate, iron, and zinc in plant and animal metabolisms (NAS 1977 Eisler 1989, 1993)... 

Proposed criteria for human health protection include drinking water concentrations less than 50 pg Mo/L, and daily dietary intakes less than 7 pg Mo/kg food — based on a 70-kg adult (Table 30.5). Molybdenum concentrations in blood of healthy people averaged 14.7 pg Mo/L, distributed between the plasma and erythrocytes. Anemic people had significantly lower blood molybdenum levels. In leukemia patients, molybdenum levels increased significantly in whole blood and erythrocytes but not in plasma (Shamberger 1979). Additional work is recommended on the use of blood in fish and wildlife as an indicator of molybdenum stress and metabolism (Eisler 1989). 

Cymbaluk, N.F., H.F. Schryver, H.F. Hintz, D.F. Smith, and J.E. Lowe. 1981. Influence of dietary molybdenum on copper metabolism in ponies. Jour. Nutr. 111 96-106. 

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