More:Molybdenum deficiency
Potentially Actionable Research
Molybdenum deficiency is more likely to be associated with upper motor neuron disease.
The paper, "Molybdenum deprivation, purine ingestion and an astrocyte-associated motor neurone syndrome in sheep: assumed clinical effects of inosine," [1] describes the "Mo-containing enzyme xanthine oxidase-dehydrogenase, which facilitates the final two steps in the catabolism of the endogenous purines to uric acid."
Molybdenum deficiency is affecting iron which then affects glutamate:
Immunohistochemical studies are required to differentiate the two. However, neither is characterised by the presence of cytoplasmic pigmented granules, which would indicate that the degenerate astrocytes associated with inosine and xanthosine are not Alzheimer-type cells and, consistent with this, the treated sheep displayed no evidence of either liver disease or encephalopathy. In the brain, the conversion of ferrous to ferric iron takes place in astrocytes and if ferrous iron accumulates in an astrocyte it will cause rupture of the cell membrane. In the affected sheep, the pigmented granules that were formed in the astrocytes’ cytoplasm had a blue-green reaction to Lillie’s Fe2+ ion uptake stain. This stain is positive (green) for melanins; however, if Fe2+ is present and the pH is acidic the colour reaction becomes blue-green,15 as in the present case. If Fe2+ had accumulated in the affected astrocytes, that may explain why they underwent degeneration and as a consequence ended their normal contribution to glutamate uptake and release. The effect of this on neuronal transmission would be to reduce glutamatergic excitation and by default increase the dominance of GABA-ergic inhibition.
References
- ↑ Bourke &: Molybdenum deprivation, purine ingestion and an astrocyte-associated motor neurone syndrome in sheep: assumed clinical effects of inosine. Aust. Vet. J. 2015;93:79-83. PMID: 25708791. DOI. 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.
