Oxidative stress is defined as the imbalance between the production
of oxidants or reactive oxygen species (ROS), such as
superoxide (O2
) and hydrogen peroxide (H2O2), and their elimination
via antioxidants, such as superoxide dismutase (SOD) and catalase.
Sustained oxidative stress results in significant destruction
of cellular structures and functions and has been implicated in
numerous pathological conditions, such as atherosclerosis, cancer,
renal disease, and diabetes [1–3]. Given that a toxic oxidative
milieu can be generated via hypoxia, cytokines, and inflammation,
cellular transplants are particularly susceptible to oxidative damage,
resulting in increased cell death and decreased efficacy of
implants [4,5]. Protecting cellular grafts from oxidative damage
due to this noxious environment is especially challenging in the
context of pancreatic islet transplantation for treatment of Type
1 diabetes mellitus, due to the inherently low gene expression
and activity of important antioxidant enzymes in pancreatic islets
[6–8]. Oxidative damage of islets following transplantation is one
of the contributing factors resulting in graft destabilization and
decreased long-term efficacy [9].