The body’s mechanism for dealing with oxidative stress becomes less efficient as we get older. This decline in function is associated with the impairment of the first enzyme (glutamate cysteine ligase or GCL). As is to be expected with any such complex system, the likelihood of errors is increased.
A dysfunctional GCL will result in insufficient γ-glutamylcysteine (GGC) being produced for the glutathione synthase enzyme to convert into glutathione (GSH). The resulting suboptimal homeostasis of glutathione (GSH) results in a decreased capacity to minimize oxidative stress, which is associated with poor outcomes during aging, inflammation and in multiple disease states.