Mizuno S, Fujita K, Furuy R, Hishid A, Ito H, Tashim Y, Kumagai H
Department of Clinical Nutrition, School of Food and Nutritional Sciences, University of Shizuoka, Japan.
Toxicology. 1997 Feb 28;117(2-3):183-91. doi: 10.1016/s0300-483x(96)03573-1.
Studies were performed to investigate the relationship between heat shock protein (HSP) and the acquired resistance to uranyl acetate (UA)-induced acute renal failure (ARF). Rats were resistant to a rechallenge with 5 mg/kg of UA between 1 and 2 weeks after the first injection of the same amount of UA. During this period, the renal HSP73 was increased to 148 +/- 12% of baseline, and tubular damage as well as an increase in serum creatinine after the second challenge of UA were significantly lower than existing after the first challenge. At 4 weeks after the first injection of UA, the amount of HSP73 returned to the normal level, and serum creatinine at the 5th day after the second challenge was increased to a level equivalent to that after the first injection. A lower dose of UA (2 mg/kg) had a little effect on the renal HSP73 content and induced limited resistance to 5 mg/kg of UA at 2 weeks after the first injection. Whole-body hyperthermia markedly increased the renal HSP72 content, but not that of HSP73, and did not induce resistance to UA. These data suggest that the increase in renal HSP73 might be associated with the acquired resistance to UA in rats, although there is no direct evidence that HSP73 produced by the regenerated cells plays a role in the acquired resistance.