Overexpression of mitochondrial manganese superoxide dismutase protects against radiation-induced cell death in the human hepatocellular carcinoma cell line HLE.

We investigated the potential role of mitochondrial manganese superoxide dismutase (Mn-SOD) in protective activity against irradiation by analyzing cell viability by a colony formation assay and by detecting apoptosis in stably human Mn-SOD gene-transfected HLE, a hepatocellular carcinoma cell line. We found that overexpression of Mn-SOD reduced the levels of reactive oxygen species in the mitochondria and intracellular phospholipid peroxidation product (4-hydroxy-2-nonenal) and prevented cell death. The production of intracellular nitric oxide after irradiation was not changed by Mn-SOD overexpression. The results suggested that Mn-SOD might play an important role in protecting cells against radiation-induced cell death by controlling the generation of mitochondrial reactive oxygen species and intracellular lipid peroxidation.

Case report: congenital absence of the portal vein associated with nodular hyperplasia in the liver.

Congenital absence of the terminal portion of the portal vein with visceral venous return to the suprahepatic inferior vena cava, a rare malformation, was demonstrated in an 18-year-old Japanese woman. She had nodular hyperplasia in the liver and a non-functioning pancreatic endocrine tumour. It is generally believed that reduction of portal venous flow causes atrophic changes and, subsequently, nodular hyperplasia occurs in a well-perfused area in the liver. However, the liver was not perfused by the portal vein in this case. It is suggested that nodular hyperplasia can occur without portal blood flow.