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The mechanism likely involves correction of oxidative stress and modulation of glutamate signaling via the cystine-glutamate antiporter (system Xc-) [73][74]

Zhuan et al

Conversely, when stimulated with 100 mM caffeine, flexor digitorum brevis myofibers from SELENON deficient mice had reduced amplitude of Ca 2+ release compared to wild-type mice which suggests that the ryanodine receptor of the SR may be impaired with loss of SELENON ( 2+ from the SR so, although it is evident that SELENON loss results in impairment of Ca 2+ homeostasis, the origin of this defect remains unclear and may involve both the release (ryanodine receptor) and re-uptake (SERCA) of Ca 2+

In the second step, glutathione synthetase (GS) catalyzes the formation of GSH by linking GGC to GLY [38,43]

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