Abstract
Glutathione is an important intracellular antioxidant in virtually all tissues, including the kidney. In the kidney, it has a rapid turnover in tubule cells and likely plays a role in any oxidant-related events which contribute to the tubule cell injury which occurs during acute renal failure. It was surprising, therefore, to find that the component amino acid, glycine, rather than glutathione itself, most strongly modulated the sensitivity of tubules cells to a variery of insults in several in vitro systems where rhese processes can be studied most directly. lhis paper reviews available evidence concerning the nature of both glutathione and glycine efects, their expression in vivo in in vitro, and their implications for understandng acute renal failure.