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Glycine cytoprotection during lethal hepatocellular injury from adenosine triphosphate depletion.

Abstract：

:Glycine protects renal tubule cells from cell death during adenosine triphosphate (ATP) depletion. Although the liver plays a key role in glycine metabolism, information is lacking regarding the effects of glycine on lethal hepatocellular injury. Thus, the aim of this study was to determine the potential cytoprotective role of glycine during ATP depletion of rat hepatocytes. Metabolic inhibition with 2.5 mmol/L potassium cyanide (KCN) was used to produce ATP depletion. Hepatocyte suspensions treated with KCN had a 2-hour viability of 5.9% +/- 2.0%, whereas cells treated with KCN in the presence of 2.0 mmol/L glycine had a viability of 80.2% +/- 1.5%, which was virtually identical to controls (81.5% +/- 1.9%). Glycine cytoprotection was dose dependent and amino acid specific. The cytoprotective effect of glycine was not mediated by protein synthesis, glycine mitochondrial metabolism, cytosolic acidosis, or preservation of either intracellular cellular glutathione or ATP. However, glycine did decrease total cellular proteolysis by 18% +/- 2%, 25% +/- 3%, and 33% +/- 1% after 1, 2, and 3 hours of KCN treatment, respectively (P less than 0.01). Inhibition of proteolysis by glycine was dose dependent over the same range as its cytoprotection. The results suggest that glycine protects against hepatocellular injury by inhibiting degradative proteolytic activity. It was concluded that proteolysis may be an important mechanism contributing to lethal injury of hepatocytes during ATP depletion.

journal_name

Gastroenterology

journal_title

Gastroenterology

authors

Dickson RC,Bronk SF,Gores GJ

doi

10.1016/0016-5085(92)90338-y

keywords:

subject

Has Abstract

pub_date

1992-06-01 00:00:00

pages

2098-107

issue

6

eissn

0016-5085

issn

1528-0012

pii

0016-5085(92)90338-Y

journal_volume

102

pub_type

杂志文章

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