Abstract
The present study was designed to investigate a role for free radical generation and lipid peroxidation in inflammation. The Koch model of Inflammation, an example of a cell-mediated hypersensitivity reaction, was induced in male Wistar albino rats to measure the presence of free radicals and products derived from lipid peroxidation from the time of challenge and thereafter, throughout the ensuing inflammatory response. Elevated levels of malondialdehyde and ethane, two products of the peroxidative decomposition of unsaturated lipid, were demonstrated during the development of foot pad inflammation. Increased levels of malondialdehyde were found to continue for at least the following 96 hours. The initiation of foot pad oedema was accompanied with the production of at least three types of active oxygen species (hydrogen peroxide, hydroxyl radical, superoxide anion), as demonstrated by intense luminol-amplified chemiluminescence. Prostaglandins were found to be elevated 6-8 hours after the onset of oedema and their presence was associated with a further rise in oedema. A significant role for free radical generation and lipid peroxidation in the development of foot pad inflammation is considered. Treatment with two anti-inflammatory agents, indomethacin and prednisolone, resulted in reduced levels of malondialdehyde and free radical generation (luminol-amplified chemiluminescence) during the evolution of foot pad oedema. These results have suggested that inhibition of oxygen derived radicals and malondialdehyde may contribute to the anti-inflammatory action of these agents. The significance of the results in relation to inflammation is discussed.