Tempol

Tempol is a superoxide scavenger that displays neuroprotective, anti-inflammatory and analgesic effects. (In Vitro) :Tempol significantly attenuates H2O2-mediated decrease in mitochondrial respiration and increase in LDH release from rat PT cells, indicating a reduction in cell injury and death. The beneficial actions of Tempol are similar to those obtained using the Fe2+ chelator DEF. However, coadministration of DEF and Tempol does not produce any additional beneficial actions against renal ischemia/reperfusion injury or against oxidative stress-mediated PT cell injury/death. (In Vivo) :SOD-mimetic Tempol is able to mimic resveratrol’s effects on heart function. Tempol is administered daily by gavage. Mice treated with Met or Tmp had decreased PR and QTc intervals and increased heart rates compared to peroral vehicle (VEH) . These results are similar to that obtained by treatment with RSV. Pre- and post-treatment profiles of individual mice are illustrated. Tempol, a membrane-permeable radical scavenger, reduces oxidant stress-mediated renal dysfunction and injury in the rat. Tempol significantly reduces the increase in urea, creatinine, γGT, AST, NAG, and FENa produced by renal ischemia/reperfusion, suggesting an improvement in both renal function and injury. Tempol also significantly reduces kidney MPO activity and MDA levels, indicating a reduction in PMN infiltration and lipid peroxidation, respectively. Tempol reduces the histologic evidence of renal damage associated with ischemia/reperfusion and caused a substantial reduction in the staining for nitrotyrosine and PARS, suggesting reduced nitrosative and oxidative stress.

2226-96-2

4-hydroxy TEMPO

>98% (HPLC)

DMSO:34 mg/mL (197.39 mM) ; Ethanol:34 mg/mL (197.39 mM) ; Water:34 mg/mL (197.39 mM)

[O]N1C (C) (C) CC (O) CC1 (C) C

C9H18NO2

172.24

Storage temperature: -20°C. Stability: ≥ 2 years

For research use only.