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Abstract
It is an established fact that animals recovering from prior acute renal failure (ARF) are resistant to subsequent renal failure challenge with the same toxic agents, although the detailed mechanisms responsible for this phenomenon remain unclear. In this study, the mechanism underlying acquired resistance to gentanmicin (GM) was investigated from the viewpoint of kidney tissue enzymology. Sprague-Dawley rats (N = 40) were administered GM subcutaneously at the dose of 80mg/day consecutively for 40 days. Blood urea nitrogen (BUN) reached the maximum mean concentration of 36 mg/dl on day 14. Thereafter, it decreased to a level within the normal range on day 21. The change in fractional excretion of sodium (FENa) showed a curve virtually identical to the change in BUN. In renal tissue, the elevation of malondialdehyde (MDA) levels was transient during continued administration of GM. The shingomyelin (SPH)/phosphatidylcholine (PC) ratio significantly decreased on day 4, but there was no marked change thereafter. The levels of total phospholipids (PLs), phosphatidylcholine (PC), and phosphatidylethanolamine (PE) increased, whereas SPH decreased mostly on day 4. The levels of phosphatidylinositol (PI) showed a continued fall during the 40 days of the experiment. On day 40, these changes in composition recovered. Phospholipase A2 (PLA2) activities decreased gradually, whereas a distinct increase in phospholipase C (PLC) activity was maintained after day 21. Furthermore, glutathione (GSH) levels also showed two distinct cycles of decrease and increase. PLs levels correlated well with PLC activities. It was concluded that accelerated lipid peroxidation occurs early in the course of GM administration and enhances changes in the phospholipid composition, which has an influence on membrane fluidity. Thus, acquired resistance to ARF induced by GM may be due to the supply of GSH and the maintenance of alteration in phospholipid composition, which are induced by PLC activities.
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