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Thus, although some of the damage in this experimental model of colitis reflects a direct erosive effect of TNBS and ethanol, their combined administration to rats reflects the in vivo operation of the damaging mechanisms elicited by TNBS, namely GSH depletion and ROS generation, indicating that ethanol facilitates the access of TNBS to the cell interior ensuring TNBS-induced GSH depletion and ROS generation

Absence of glutathione peroxidase-1 exacerbates cerebral ischemia-reperfusion injury by reducing post-ischemic microvascular perfusion