Cysteine and cobalamin
The piece of the dissertation below may explain the success of Selenite in treating B12 deficiency. This is unrelated to thyroid hormone or B2 activation, but about GSH/GSSG (Redox status).
In short: Cobalamin status in the brain favours Cysteine-rich AND Selenium-rich cells in the brain:
“**Together, these results suggest that low selenium and low cysteine culture condition could impair neuronal Cbl uptake.
The influence of cysteine and selenium on levels of active Cbl species was further examined.
Levels of AdoCbl and MeCbl were significantly decreased by low cysteine (100ĀµM) and low selenium culture (1nM) condition (Fig. 41), indicating thatĀ low selenium and low cysteine culture conditions impaired neuronal synthesis of active Cbl species
Interestingly, the level of AdoCbl was decreased by about 60% when the selenium concentration was reduced from 100nM to 10nM at the cysteine concentration of 1mM,Ā but at a cysteine concentration of 100ĀµM, AdoCbl level was not affected by such reduction of selenium concentration.” (R1)
So Cysteine is important for the activation of cobalamin.
“This may suggest that when the antioxidants are limited in the culture media, compensatory mechanisms in cells can be activated to maintain the AdoCbl level.
On the other hand, the MeCbl level appeared to be more sensitive to changes of both seleniumĀ and cysteine concentrations, with a decrease of up to 85% (Fig. 41b).
The cysteine concentration appeared to have a more profound effect on the MeCbl level than selenium, since the same fold reduction of cysteine concentration induced a greater decrease in the level of MeCbl” (R1)