• Yuji Okatani, Akihiko Wakatsuki, Hideaki Enzan, and Yasuyo Miyahara.
• Department of Clinical Nursing Science, Kochi Medical School, Oko, Nankoku, Kochi 783-8505, Japan. okataniy@med.kochi-ms.ac.jp
• Eur. J. Pharmacol. 2003 Mar 28;465(1-2):163-70.

AbstractThis study investigated the effects of edaravone (3-methyl-1-phenyl-2-pyrazolin-5-one, MCI-186), a potent free radical scavenger, on the prevention of mitochondrial injury induced by hepatic ischemia and reperfusion. Mature male rats were subjected to 70 min of hepatic ischemia and 2 h of reperfusion. The rats received vehicle or edaravone (10 mg/kg body weight) intravenously prior to ischemia, before reperfusion and 1 h after reperfusion. In the vehicle-treated animals, the respiratory control index, ADP/O, State 3 respiration and dinitrophenol-induced uncoupled respiration decreased markedly after ischemia/reperfusion and were restored by edaravone administration. Mitochondrial lipid peroxidation was elevated in the vehicle-treated group, which was attenuated by edaravone, while mitochondrial glutathione peroxidase activity decreased in the vehicle-treated group, which was similarly abrogated by edaravone treatment. Electron microscopic observation demonstrated that treatment with edaravone restored the ischemia/reperfusion-induced disorganization of mitochondrial structures. Edaravone protects against mitochondrial injury, which prevents mitochondrial oxidative stress and improves ischemia/reperfusion-induced hepatic energy metabolism.

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