Cyclosporin a increases hypoxia and free radical production in the rat kidney: prevention by dietary glycine1. Zhong, Zhi, Gavin E. Arteel, Henry D. Connor, Ming Yin, Moritz V. Frankenberg, Robert, F. Stachlewitz, James A. Raleigh, Ronald P. Mason and Ronald G. Thurman,. 2Depts. of Pharmacology and 4Radiation Oncology, 3Curriculum in Toxicology, Univ. of North Carolina at Chapel Hill, NC 27599 and 5Lab. Of Pharmacology and Chemistry, NIEHS, RTP, NC 27709
APStracts 5:0133F, 1998.
The major side effect of cyclosporin A is severe nephrotoxicity. It is likely that cyclosporin A causes vasoconstriction leading to hypoxia -reperfusion injury; therefore, these experiments were designed to attempt to obtain physical evidence for hypoxia and free radical production in kidney following cyclosporin A. Rats were treated daily with cyclosporin A (25 mg/kg, p.o.) for 5 days, and pimonidazole, a hypoxia marker, was injected 2 hours after the last dose of cyclosporin A. POBN ((-(4-pyridyl 1-oxide)-N-tert-butylnitrone) was injected 3 hours after cyclosporin A to trap free radicals. Cyclosporin A doubled serum creatinine and decreased glomerular filtration rates by 65% as expected. Pimonidazole adduct binding in the kidney was increased nearly 3-fold by cyclosporin A, providing physical evidence for tissue hypoxia. Moreover, cyclosporin A increased POBN/radical adducts nearly 6-fold in the urine but did not alter levels in the serum. Glycine, which causes vasodilatation and prevents cyclosporin A toxicity, minimized hypoxia and blocked free radical production; however, it did not alter cyclosporin A blood levels. These results demonstrate for the first time that cyclosporin A causes hypoxia and increases production of a new free radical species exclusively in the kidney. Therefore, it is concluded that cyclosporin A causes renal injury by mechanisms involving hypoxia -reoxygenation, effects which can be prevented effectively by dietary glycine.

Received 1 October 1997; accepted in final form 30 July 1998.
APS Manuscript Number F318-7.
Article publication pending Am. J. Physiol. (Renal Physiology).
ISSN 1080-4757 Copyright 1998 The American Physiological Society.
Published in APStracts on 21 September 1998