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Even though our data show that both agents separately caused cell damage, ethanol potentiated the mucosal injury caused by TNBS, an event that was accompanied by a significant depletion of mucosal GSH levels, suggesting that GSH limitation contributed to enhanced cell injury (Table 1)

Depletion of GSH can lead to, among other things, mitochondrial dysfunction and cell death

Temporal increases in plasma markers of oxidized low-density lipoprotein strongly reflect the presence of acute coronary syndromes

Recent studies have identified several key regulators of astrocytic antioxidant functions, including the mGLUT3 receptor, cyclic AMP, ROS-induced mitochondrial DNA release and dystrophin 85,86

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