CASP3 and acute kidney injury: In general, the mechanisms underlying nephrotoxicity are: (a) kidney-specific mitochondrial oxidative stress, caused by altered activities of mitochondrial electron transport chain enzyme complexes and accompanied by impaired antioxidant defenses, (b) inflammation, as evidenced by elevated levels of inflammatory mediators, such as TNF-α, IL-1, increased activities of NF-κB and p53 induction, and (c) apoptotic cell death, as indicated by high caspase-3 activity and DNA fragmentation in diverse clinical and experimental studies of AKI [100,101].