Mito-TEMPO, a mitochondria-targeted superoxide dismutase mimetic, scavenges superoxide and alkyl radicals, preventing mitochondrial oxidation, necrosis, and apoptosis.

METHODS: Human neuroblastoma cells SH-SY5Y were treated with Mito-TEMPO (25-100 μM) for 24 h. Cell viability was detected using MTT assay.
RESULTS: No cytotoxic effect was shown on the cells in the Mito-TEMPO-treated group, and a significant increase in cell viability was detected after Mito-TEMPO treatment. [1]
METHODS: Normal rat proximal renal tubular epithelial cell line NRK-52E was pretreated with Mito-TEMPO (10 μM) for 1 h, then stimulated with oxalate (700 μM) for 1 h. The mitochondrial membrane potential was detected by using MMP assay kit (JC-1).
RESULTS: The control cells showed bright red fluorescence. Compared with the control, oxalate treatment attenuated the red fluorescence, and these changes were reversed by pretreatment with Mito-TEMPO. The RESULTS suggest that oxalate induces mitochondrial dysfunction, and Mito-TEMPO can inhibit this effect. [2]

METHODS: To investigate the protective effect against hepatotoxicity, APAP (300 mg/kg) was intraperitoneally injected into C57BL/6J mice, and Mito-TEMPO (20 mg/kg in saline) was injected intraperitoneally 1.5-3 h later.
RESULTS: Mito-TEMPO had a protective effect on the late hepatotoxicity of APAP. [3]
METHODS: To investigate the effects on coronary vasodilatation and endothelial SK channel activity, Mito-TEMPO (1 mg/kg in saline) was intraperitoneally injected into C57BL/6J mice with or without diabetes once daily for four weeks.
RESULTS: After 4 weeks of treatment with Mito-TEMPO, diabetic mice showed significantly improved endothelium-dependent diastolic responses of coronary arteries to ADP or NS309 and endothelial SK channel currents compared to untreated diabetic mice. [4]