Liposome-mediated augmentation of superoxide dismutase in endothelial cells prevents oxygen injury.

摘要: Increased intracellular production of oxygen radicals is a major etiology cell damage from many quinoid antibiotics, environmental toxicants, and hyperoxia. Enhancing the content protective enzymes can provide means limiting biological caused by free radicals. Liposomal entrapment delivery superoxide dismutase to cultured porcine aortic endothelial cells increased specific activity cellular 6 12-fold. This augmented persisted in monolayers rendered these resistant oxygen-induced injury. Culture confluent hyperoxia 51Cr lactate dehydrogenase release an concentration-dependent manner. Superoxide dismutase-augmented were compared untreated controls, Free absence or presence liposomes containing no enzyme had effect on did not protect damage. Liposomes made saturated fatty acid-containing phospholipids small but significant These probably membrane lipid thereby decreased peroxidative when exposed Conversely, preincubation with arachidonic acid content, sensitivity hyperoxia, hyperoxia-induced thiobarbituric material. data suggest that prevents important mediator toxicity.