Severe total hepatic ischemia and reperfusion: Relationship between very high α-tocopherol uptake and lipid peroxidation

Abstract

Reperfusion injury of the liver occurs in liver transplantation and in major hepatectomies. It triggers a severe oxidative stress that leads to increased lipid peroxidation. In our study we examined the effect of parenteral supranutritional administration of α-tocopherol, a vitamin that plays a key role in the endogenous antioxidant system, to rats subjected to severe ischemia/reperfusion (I/R) injury of the liver. α-Tocopherol was administered to the animals at doses of 30 and 300mg/kg bw, whereas total hepatic ischemia was induced for 60 min followed by 120 min reperfusion. Tissue and blood samples were collected for malonyldialdehyde (MDA) and serum α-tocopherol assay, respectively. In the sham operation group, mean MDA level in liver was 1.14nmole/g wet tissue in the control subgroup, and 1.01 or 0.74nmole/g wet tissue in the subgroups given 30 or 300mg/kg α-tocopherol. In the I/R group, mean MDA level was 1.57nmole/g wet tissue in the control subgroup, and 0.97 and 0.77nmole/g wet tissue in the subgroups given 30 or 300mg/kg α-tocopherol. Mean levels of α-tocopherol in serum (μmole/l) were 10.20 and 1.80 in the control subgroups, 25.28 and 11.25 in the subgroups treated with 30 and 300mg/kg bw of α-tocopherol, and 31.00 and 13.02 in the subgroups treated with 30 and 300mg/kg bw of α-tocopherol, within the sham-operation and I/R groups, respectively. A significant decrease of MDA accompanied by a significant increase of serum α-tocopherol was documented in the α-tocopherol-treated rats within both groups. Ischemia/reperfusion triggered a significant increase of the MDA level in the liver of the rats not treated with α-tocopherol as compares with the treated animals.