Up to now, hypovolemia and low cardiac output were thought to be the major etiologic factors in acute renal failure in massive burn.
The aim of this study was to prove the role of oxygen-derived free radicals as mediators of the direct renal tissue damage in massive burn.
The most damaging effect of free radicals is lipid peroxidation.
The malondialdehydes, usually used as a marker of lipid peroxidation, were quantified in rat kidnies for the following condition: control, only burn injury. and burn injury plus pretreatment with superoxide dismutase(a superoxide anion
scavenger),
mannitol(a hydroxyl radical scavenger), allopurinol(a xanthin oxidase inhibitor).
In unpretreated case, burn injury significantly significantly increased the level of malondialdehyde in rat kidney tissue from 0.58±0.06μml/gm of tissue(control) to 1.76±0.2μml/gm of tissue.
However, pretreated with allopurinol(0.77±0.14μml/gm of tissue), mannitol(0.75±0.12μml/gm of tissue), superoxide dismutase(0.68±0.1μml/gm of tissue) significantly decreased the amount of lipid peroxidation of massive burned rat kidney.
Both light and electron microscopic finding also showed the decreased renal tissue damage in pretreated cases.
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