AI Article Synopsis
- The study explored how a compound called MnTMPyP affects mitochondrial function during kidney injury caused by restricted blood flow and subsequent restoration, known as renal ischemia-reperfusion injury (IRI).
- Results indicated that MnTMPyP helped preserve important mitochondrial activities and structures during the early stages of reperfusion, indicating a protective role.
- Additionally, after 24 hours of reperfusion, MnTMPyP effectively reduced cell death (apoptosis) by blocking a key enzyme, supporting its potential as a therapeutic agent in renal IRI.
Article Abstract
This study examined the time-dependent effects of a cell permeable SOD mimetic, MnTMPyP, on mitochondrial function in renal ischemia-reperfusion injury (IRI). Male SD rats were subject to either sham operation or bilateral renal ischemia for 45 min followed by reperfusion for 1, 4 or 24 h. A sub-set of animals was treated with either saline vehicle or 5 mg/Kg of MnTMPyP (i.p.). EPR measurements showed that at 1-h reperfusion MnTMPyP prevented a decrease in aconitase activity (p < 0.05) and attenuated the increase in the high spin heme at g = 6 and oxidation of 4Fe4S to 3Fe4S signal at g = 2.015 (p < 0.01). MnTMPyP was effective in preventing loss of mitochondrial complexes and prevented the loss of cytochrome c and Smac/Diablo from mitochondria early in reperfusion. Following 24 h of reperfusion MnTMPyP was effective in attenuating caspase-3 and blocking apoptosis (p < 0.05). In conclusion, MnTMPyP has biphasic effects in renal IRI, inhibiting mitochondrial dysfunction at the early phases of reperfusion and prevention of apoptosis following longer durations of reperfusion.
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| http://dx.doi.org/10.3109/10715761003786164 | DOI Listing |
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