O2-. release by activated Kupffer cells upon hypoxia-reoxygenation.

Primary cultures of rat liver Kupffer cells generated large amounts of superoxide anion radical (O2-.) when subjected to reoxygenation after a hypoxic period of at least 2 h. O2-.

Hypoxia/reoxygenation injury in liver: Kupffer cells are much more vulnerable to reoxygenation than to hypoxia.

Cell injury due to hypoxia and reoxygenation was studied in primary cultured rat Kupffer cells. Under hypoxic conditions only 20% of the cells had lost their viability after 12 h of incubation. In contrast, almost complete losses of cell viability were observed when reoxygenation was performed after 2, 4 or 6 h of hypoxia.

Partial purification of rat liver microsomal glucose-6-phosphatase on hydroxylapatite.

Glucose-6-phosphatase was effectively solubilized from rat liver-microsomal membrane by the nonionic detergent Renex 690 in the presence of 0.6M sodium chloride. Subsequent separation on hydroxylapatite proved to be a successful and rapid initial step towards the purification of this enzyme.

Alterations of the microsomal glucose-6-phosphatase system evoked by ferrous iron- and haloalkane free-radical-mediated lipid peroxidation.

Alterations of catalytic activities of the microsomal glucose-6-phosphatase system were examined following either ferrous iron- or halothane (CF3CHBrCl) and carbon tetrachloride (CCl4) free-radical-mediated peroxidation of the microsomal membrane. Enzyme assays were performed in native and solubilized microsomes using either glucose 6-phosphate or mannose 6-phosphate as substrate. Lipid peroxidation was assessed by the amounts of malondialdehyde equivalents formed.