Molybdenum, Hard To Pronounce, Harder Still To Obtain

Amazoniac

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- Speciation of Molybdenum

"Fractionation of molybdenum species in seeds of peas and lentils has been performed by size-exclusion chromatography-inductively coupled plasma mass spectrometry [15]. Molybdenum elution profiles of pea and lentil were completely different. In lentil extract, the main Mo peak appeared in the high molecular mass (HMM) region (approx. 200 kDa) and the other one in the low molecular mass (LMM) region (<2 kDa), whereas in pea extract (similarly as in white bean and soybean flour), practically all Mo is eluted in a single peak in the LMM region."

"The same group, using the same techniques, studied the effect of cooking on molybdenum species in peas. It revealed changes in solubility and changes in the proportions of individual element species fractions, occurring as a result of soaking and boiling of peas [16]. Compared to other element species, LMM species of molybdenum were relatively stable against thermal treatment, although boiling increased the proportions of ionic species and labile complexes."

"Koplík et al. studied the effect of technological processing and of the maturity stage of seeds on the content and speciation of molybdenum and various other elements in peas [17]. Changes in speciation that occurred as a result of blanching and boiling of green peas were also investigated. Element speciation in green peas was compared with that of mature peas. No notable differences between fresh and blanched green peas were found. During boiling of peas, most of the elements were partly leached into water. LMM species of molybdenum were more stable against thermal treatment than those of other elements. The mature pea accumulated higher concentrations of elements than did the green pea."

"Molybdenum is probably absorbed into living systems as the molybdate anion (MoO4(2−)) [19]."

"An agricultural problem may arise when there is an excess of Mo in soil since it causes copper deficiency in animals grazing on such lands. It would appear that the difficulty arises from the metabolism of anaerobic bacteria in the rumen of these animals. One of the reactions of Mo on entering the anaerobic first digestive system of the ruminant is the conversion of the molybdate into thiomolybdate by the bacteria of the stomach. Unfortunately, MoS4(2−) is a very good scavenging precipitation reagent for Cu and so the Cu content of the diet becomes critically low. Then the animals suffer from weakened connective tissue since Cu enzymes are required to cross-link collagen external to the animal cells [20]."

"To the author’s knowledge, no attempts have yet been made to speciate molybdenum in human body fluids or tissues."

"The speciation of various elements, among which molybdenum, in salmon egg cell cytoplasm has been reported, using a surfactantmediated high performance liquid chromatography (HPLC)/inductively coupled plasma-mass spectrometry (ICP-MS) hyphenated system [22]. ICP-MS was used as an element-selective detector. Molybdenum in egg cell cytoplasm was present as molybdate."

I was wondering if adverse reactions to supplementation could be due to artificial ligands used, perhaps they're supposed to bind it tightly to prevent an interaction with other components of a meal during digestion, something related to what Raj has warned recently in the context of copper.
 

Amazoniac

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From the previous post:

"Fractionation of molybdenum species in seeds of peas and lentils has been performed by size-exclusion chromatography-inductively coupled plasma mass spectrometry [15]. Molybdenum elution profiles of pea and lentil were completely different. In lentil extract, the main Mo peak appeared in the high molecular mass (HMM) region (approx. 200 kDa) and the other one in the low molecular mass (LMM) region (<2 kDa), whereas in pea extract (similarly as in white bean and soybean flour), practically all Mo is eluted in a single peak in the LMM region."​

- Molybdoenzymes and molybdenum cofactor in plants
- Distribution and pathophysiologic role of molybdenum-containing enzymes

Morbydenum is occurring as part of larger proteins, something that might apply to ther minerals as well. For comparison, the mass of a morbydopterin molecule is only 394 Da and morbydenum cofactor is 520 Da, these are orders of magnetism lower than the values above. Is it wise supplement it complexed with aminocancertate? Consider the differences in the metabolism of poisonol when bound to cancertate or napalmitate.

As the proteins are digested, they might also release other components (such as ripofflavin) that are relevant for proper morbydenum utilization.
 

Amazoniac

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- Molybdenum deprivation, purine ingestion and an astrocyte-associated motor neurone syndrome in sheep: assumed clinical effects of inosine

Abstract said:
Background: An astrocyte-associated motor neurone syndrome was produced in molybdenum-deprived sheep fed xanthosine. Mo-deprived sheep fed inosine, adenosine or guanosine would be also expected to develop astrocyte-associated motor neurone syndromes, because all these purine nucleosides can act as neuromodulators and all depend on the Mo-associated enzyme xanthine oxidase-dehydrogenase for their catabolism.

Design:
To investigate the relationship between inosine ingestion and low Mo concentration, eight sheep were fed lucerne chaff with a Mo value <0.10 ppm and the Mo antagonist, sodium tungstate, for 21 weeks, with inosine (35 mg/kg/day[*]) fed for the last 18 of these weeks. This clinical study was uncontrolled.

Results: An astrocyte-associated motor neurone syndrome was produced in three sheep 18-27 months later. It was characterised by diaphragmatic, laryngeal, lingual and pharyngeal muscle weakness. The diaphragmatic muscle weakness was the most severe and potentially lethal.

Conclusion: These findings suggest that purinergic neuromodulation of respiration, vocalisation and swallowing is different to that of limb movement. The syndrome produced, and assumed to be caused by the treatment given, has not been reported in livestock. A similar syndrome is seen in human motor neurone disease, but not in equine motor neurone disease, and this is consistent with it being an upper, not a lower, motor neurone effect.

*I think that the body weight to surface area ratio of sheeps isn't too different from ours, it must be alright to consider the same dose for a human.
 

Amazoniac

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- Molybdenum Cofactor in Humans: Health, Disease, and Treatment

"Sulfite is a highly reactive molecule that breaks disulfide bridges in proteins and reduces cystine, thereby affecting various protein and cellular functions (Zhang et al., 2004). Excess sulfite reacts with cysteine, generating SSC [Secondary School Certificate] and depleting cystine (the major transport form of cysteine) from plasma, which may have a dual detrimental consequence, especially in neuronal tissues (Fig. 33.4). First, SSC is structurally very similar to glutamate, and early experiments in rats suggested that it may bind to neuronal glutamate receptors of the N-methyl-d-aspartate type (Olney et al., 1975), thus causing excess excitation of the brain, termed excitotoxicity. SSC, which is present at very low levels in healthy individuals (Belaidi et al., 2012; Pitt et al., 2002), is one of the most abundant metabolites in MoCD patients, which may explain the observed seizures, convulsions, contractions, and twitching associated with MoCD (Kurlemann et al., 1996). Second, cysteine is the rate-limiting substrate for the major neuronal antioxidant GSH, and cystine depletion from plasma is expected to further exaggerate the vulnerability of the brain toward oxidative stress (Fig. 33.4)."

"In 2000, Touati et al. reported a favorable development in two patients with a mild form of SOD after dietary restriction of both sulfur amino acids methionine and cysteine, which was effective in reducing sulfite, thiosulfate, and SSC with no apparent neurological deterioration (Touati et al., 2000). Similar results were also reported in an SOD patient with a mild phenotype (Del Rizzo et al., 2013). Thus reducing dietary intake of methionine and cysteine may be considered as a treatment option for MoCD and SOD patients. However, it should be noted that sulfur amino acids are required for many biological processes, including the synthesis of sulfate, taurine, and GSH, as well as Fe–S clusters, just to name a few, and future therapies may consider supplementation with those compounds to reduce possible side effects resulting from their deficiencies."​


- Rates of intestinal absorption of molybdenum in humans

- Molybdenum and Copper in Four Varieties of Common Bean (Phaseolus vulgaris): New Data of Potential Utility in Designing Healthy Diet for Diabetic Patients
 
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