Restriction of hypoxic membrane defect by glycine improves mitochondrial and cellular function in reoxygenated renal tubules.

Abstract

The hypoxic tolerance of renal tubular cells may be improved by specific amino acids. In studies on the protective role of glutathione Weinberg and co-workers (1987) observed that not the tripeptide GSH, but one of its components, the amino acid glycine, suppressed hypoxic alterations in isolated tubular segments of rabbit renal cortex. Later experiments confirmed the cytoprotective role of short-chained, non-essential, neutral amino acids such as glycine or alanine (Heyman et al., 1992). The exact mechanism of glycine protection, however, remains unclear. Some authors postulated an unspecific (Baines et al., 1990) or ligand-bound (Weinberg et al., 1990) membrane-stabilizing effect of glycine and related compounds. Recently we reported that glycine supports cellular volume regulation in renal cortical cells at low extracellular oxygen tension (PO 2 < 1 mm Hg) as well as in a subsequent reoxygenation period (Gronow et al., 1990).