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Am J Physiol Renal Physiol 258: F346-F355, 1990;
0363-6127/90 $5.00
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AJP - Renal Physiology, Vol 258, Issue 2 346-F355, Copyright © 1990 by American Physiological Society

ARTICLES

Ouabain-induced lethal proximal tubule cell injury is prevented by glycine

J. M. Weinberg, J. A. Davis, M. Abarzua, R. K. Smith and R. Kunkel
Department of Internal Medicine, Veterans Administration Medical Center, Ann Arbor, Michigan.

Exposure to 1 mM ouabain for greater than 30 min caused lethal cell injury to isolated rabbit proximal tubules as measured by increased lactate dehydrogenase release. Addition of 2 mM glycine or glutathione to the incubation medium prevented this injury and a sharp fall of cell ATP that accompanied it. Glycine and glutathione did not alter rapid, early effects of ouabain to deplete cell K+ and inhibit respiration. Preservation of cellular glutathione was not required for protection. Glycine did not ameliorate ouabain-induced increases of cell water and did not prevent lethal cell injury associated with cell swelling produced by incubation in a high K+ concentration medium. In contrast, 100 mM mannitol, which at least partially ameliorated swelling in both ouabain and high-K+ medium, prevented lethal injury in high-K+ medium and decreased it in the presence of ouabain. The combination of glycine and mannitol completely prevented ouabain-induced lethal injury and cell water increases. These observations indicate that glycine, unlike mannitol, does not protect against primary volume-induced insults. Ouabain-induced lethal cell injury results from a process that includes both a volume component ameliorated by mannitol and a volume-independent component that is prevented by glycine and is closely associated with accelerated ATP depletion.


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