Fructose protects hepatocytes during hypoxia by inhibiting the mitochondrial permeability transition

W. Irwin, Lawrence Gaspers, J. Thomas

Research output: Contribution to journalArticle

Abstract

Fructose (but not glucose) exerts a protective effect on hepatocytes during hypoxia. This effect has been attributed to the ability of fructose to (a) provide ATP via glycolysis, and (b) cause cytosolic acidification. However, both fructose and its metabolite D-glyceraldehyde (D-GA) have little effect on cellular ATP during chemical hypoxia. Both glyceraldehyde isomers (D-GA, L-GA) protect hepatocytes as welt or better than fructose during chemical hypoxia, even though L-GA produces half the ATP as D-GA or fructose. This indicates that (a) protection involves factors other than provision of glycolytic ATP. Also, (b) both D-GA and L-GA still improve hepatocyte viability if intracellular acidosis is prevented with ionophores. Both glyceraldehyde isomers were found to inhibit swelling in isolated mitochondria under conditions that induce the mitochondrial permeability transition (MPT). Glyceraldehyde inhibition of mitochondrial swelling can be abolished by the calcium ionophore A23187. Protection by glyceraldehyde thus involves prevention of MPT by interfering with mitochondrial calcium uptake.

Original languageEnglish (US)
JournalFASEB Journal
Volume11
Issue number9
StatePublished - Dec 1 1997
Externally publishedYes

All Science Journal Classification (ASJC) codes

  • Biotechnology
  • Biochemistry
  • Molecular Biology
  • Genetics

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