Tempol is a redox-cycling
nitroxide that promotes the metabolism of many
reactive oxygen species (ROS) and improves
nitric oxide bioavailability. It has been studied extensively in animal models of oxidative stress.
Tempol has been shown to preserve mitochondria against oxidative damage and improve tissue oxygenation.
Tempol improved
insulin responsiveness in models of
diabetes mellitus and improved the
dyslipidemia, reduced the
weight gain and prevented diastolic dysfunction and
heart failure in fat-fed models of the
metabolic syndrome.
Tempol protected many organs, including the heart and brain, from
ischemia/
reperfusion damage.
Tempol prevented podocyte damage, glomerulosclerosis,
proteinuria and progressive loss of renal function in models of
salt and mineralocorticosteroid excess. It reduced brain or spinal cord damage after
ischemia or
trauma and exerted a spinal
analgesic action.
Tempol improved survival in several models of
shock. It protected normal cells from radiation while maintaining radiation sensitivity of
tumor cells. Its paradoxical
pro-oxidant action in
tumor cells accounted for a reduction in spontaneous
tumor formation.
Tempol was effective in some models of neurodegeneration. Thus,
tempol has been effective in preventing several of the adverse consequences of oxidative stress and
inflammation that underlie radiation damage and many of the diseases associated with aging. Indeed,
tempol given from birth prolonged the life span of normal mice. However, presently
tempol has been used only in human subjects as a topical agent to prevent radiation-induced
alopecia.