• Woo-Yong Lee and Sun-Mee Lee.
• College of Pharmacy, Sungkyunkwan University, Suwon, Korea.
• Arch Pharm Res. 2005 Dec 1;28(12):1392-9.

AbstractThis study evaluated the effect of alpha-tocopherol (alpha-TC), ischemic preconditioning (IPC) or a combination on the extent of mitochondrial injury caused by hepatic ischemia/reperfusion (I/R). Rats were pretreated with alpha-TC (20 mg/kg per day, i.p.) for 3 days before sustained ischemia. A rat liver was preconditioned with 10 min of ischemia and 10 min of reperfusion, and was then subjected to 90 min of ischemia followed by 5 h or 24 h of reperfusion. I/R increased the aminotransferase activity and mitochondrial lipid peroxidation, whereas it decreased the mitochondrial glutamate dehydrogenase activity. alpha-TC and IPC individually attenuated these changes. alpha-TC combined with IPC (alpha-TC+IPC) did not further attenuate the changes. The mitochondrial glutathione content decreased after 5 h reperfusion. This decrease was attenuated by alpha-TC, IPC, and alpha-TC+IPC. The significant production of peroxides observed after 10 min reperfusion subsequent to sustained ischemia was attenuated by alpha-TC, IPC, and alpha-TC+IPC. The mitochondria isolated after I/R were rapidly swollen. However, this swelling rate was reduced by alpha-TC, IPC, and alpha-TC+IPC. These results suggest that either alpha-TC or IPC reduces the level of mitochondrial damage associated with oxidative stress caused by hepatic I/R, but alpha-TC combined with IPC offers no significant additional protection.

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