Inhibition of ERK1/2 Activation by Phenolic Antioxidants Protects Kidney Tubular Cells During Cold Storage

Abstract

The results suggest that chilling of renal epithelial cells induces ROS generation by NADPH oxidase, which leads to rapid activation of the MEK-ERK1/2 cascade and initiation of cell injury. This can be prevented by antioxidants.

NADPH Oxidase-Mediated Redox Signaling: Roles in Cellular Stress Response, Stress Tolerance, and Tissue Repair

“…These observations are summarized in Table 1. In renal tubular epithelial cells, prolonged cold storage at 4°C induced ROS generation by Nox and subsequent activation of ERK1/2 ( Karhumä ki et al, 2007). Similar observations of cold storage-induced Nox activation were also reported in liver Kupffer cells (Shibuya et al, 1997).…”

Role of mitochondrial-derived oxidants in renal tubular cell cold-storage injury

“…However, MnSOD overexpression did not affect superoxide levels during RW which were already restored to basal levels from the CS-induced peak (141.8 ± 11.7 CS.RW+MnSOD vs. CS.RW 130.2 ± 6.9 mean fluorescence intensity) (Figure 1A, B). As mentioned previously, superoxide can also be generated by non-mitochondrial sources including NADPH oxidases [33]. We evaluated this possibility by treating NRK cells with diphenyleneiodonium chloride (DPI, 1 μM), a non-selective NADPH oxidase inhibitor for 1 h prior to and during CS.…”

Influence of Oxygen Concentration During Hypothermic Machine Perfusion on Porcine Kidneys From Donation After Circulatory Death

“…Such differential damaging of these important structures will contribute to the function of organs during reperfusion. Indeed, tubular cells were described as highly susceptible to hypoxia before (13), supporting the application of oxygen during HMP.…”