Permanent pancreatic islet cell destruction occurs in
type 1 diabetes mellitus (T1DM) through the infiltration of inflammatory cells and
cytokines. Loss of β-cell integrity secondary to oxidation leads to an inability to appropriately synthesize and secrete
insulin. Allogenic islet cell
transplantation (ICT) has risen as a therapeutic option to mitigate problematic
hypoglycemia. Nevertheless, during the process of
transplantation, islet cells are exposed to oxidatively
caustic conditions that severely decrease the islet cell yield. Islet cells are at a baseline disadvantage to sustain themselves during times of metabolic stress as they lack a robust
anti-oxidant defense system,
glycogen stores, and vascularity. The Nrf2/Keap1 system is a master regulator of
antioxidant genes that has garnered attention as pharmacologic activators have shown a protective response and a low side effect profile. Herein, we present the most recently studied Nrf2/Keap1 activators in pancreas for application in ICT: Dh404,
dimethyl fumarate (DMF), and
epigallocatechin gallate (EGCG). Furthermore, we discuss that Nrf2/Keap1 is a potential target to ameliorate oxidative stress at every step of the Edmonton Protocol.