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Since selenium supplementation in the forms of sodium selenite and SeM was well documented to induce the expressions of seleno-GPxs through their metabolic assimilation into bioavailable selenium (hydrogen selenide), the initial studies focused on exploring selenium supplementation as a strategy to achieve protection against radiation-induced toxicity [38, 66]
The present work hence pursued the question how intracellular glutathione can be elevated transiently to render cells more resistant toward harmful conditions
The clinical value of most of the so far described Nrf2 activators however was rather limited, mostly due to undesired interactions of these electrophiles with other cellular targets
As mentioned above, a number of compounds or drug formulations have been investigated with regard to inhibiting cysteine metabolism, either by targeting H 2 S-synthesising trans-sulphuration pathway enzymes (e.g
