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Citations to this article

Cytoprotective effects of glycine and glutathione against hypoxic injury to renal tubules.
J M Weinberg, … , M Abarzua, T Rajan
J M Weinberg, … , M Abarzua, T Rajan
Published November 1, 1987
Citation Information: J Clin Invest. 1987;80(5):1446-1454. https://doi.org/10.1172/JCI113224.
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Research Article

Cytoprotective effects of glycine and glutathione against hypoxic injury to renal tubules.

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Abstract

Roles for both the tripeptide, GSH, and individual amino acids in modifying the cellular response to oxygen deprivation-induced injury have been suggested by prior work in kidney and other tissues, but the precise interrelationships have not been clearly defined. We have studied the effects of GSH, its component amino acids, and related compounds on the behavior of isolated renal proximal tubules in a well characterized model of hypoxic injury in vitro. GSH, the combination of cysteine, glutamate, and glycine and glycine alone, when present in the medium during 30 min hypoxia, a duration sufficient to produce extensive irreversible injury in untreated tubules, were protective. Significant effects were detected at 0.25 mM concentrations of the reagents, and protection was nearly complete at concentrations of 1 mM and above. Glutamate and cysteine alone were not protective. The exogenous GSH added to the tubule suspensions was rapidly degraded to its component amino acids. Treatment of tubules with GSH or cysteine, but not glycine, increased intracellular GSH levels. Oxidized GSH was protective. Serine, N-(2-mercaptopropionyl)-glycine, and a panel of agents known to modify injury produced by reactive oxygen metabolites were without benefit. These observations identify a novel and potent action of glycine to modify the course of hypoxic renal tubular cell injury. This effect is independent of changes in cellular GSH metabolism and appears to be unrelated to alterations of cell thiols or reactive oxygen metabolites. Further elucidation of its mechanism may provide insight into both the basic pathophysiology of oxygen deprivation-induced cell injury and a practical way to ameliorate it.

Authors

J M Weinberg, J A Davis, M Abarzua, T Rajan

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Total citations by year

Year: 2025 2024 2023 2022 2021 2020 2019 2018 2017 2016 2015 2014 2013 2012 2011 2010 2009 2008 2007 2006 2005 2004 2003 2002 2001 2000 1999 1998 1997 1996 1995 1994 1993 1992 1991 1990 1989 1988 Total
Citations: 2 1 4 3 2 3 3 1 3 3 1 4 2 7 5 4 7 4 2 3 7 7 12 5 7 8 5 8 15 9 9 12 8 15 7 9 1 2 210
Citation information
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Citations to this article in year 2012 (7)

Title and authors Publication Year
Pathophysiology of Acute Kidney Injury
DP Basile, MD Anderson, TA Sutton
Comprehensive Physiology 2012
Systems Biology, Metabolomics, and Cancer Metabolism
M Tomita, K Kami
Science 2012
Short-Term Changes of the Urine Metabolome After Bariatric Surgery
N Friedrich, K Budde, T Wolf, A Jungnickel, A Grotevendt, M Dreßler, H Völzke, M Blüher, M Nauck, T Lohmann, H Wallaschofksi
OMICS: A Journal of Integrative Biology 2012
Ezrin functionality and hypothermic preservation injury in LLC-PK1 cells
T Tian, SL Lindell, M Lam, MJ Mangino
Cryobiology 2012
Glycine, a simple physiological compound protecting by yet puzzling mechanism(s) against ischaemia-reperfusion injury: current knowledge
F Petrat, K Boengler, R Schulz, H Groot
British Journal of Pharmacology 2012
Antioxidant and cytoprotective effects of L-Serine on human endothelial cells
MN Maralani, A Movahedian, SH Javanmard
Research in Pharmaceutical Sciences 2012
Natural compounds as inducers of cell death
M Diederich, K Noworyta
2012

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