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 variety of insults in several in vitro systems where these processes can be studied most directly. This paper reviews available evidence concerning the nature of both glutathione and glycine effects, their expression in vivo in in vitro, and their implications for understanding acute renal failure.
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Joel M. Weinberg (1992) studied this question.
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