Environmental Stress Causes Oxidative Damage to Plant Mitochondria Leading to Inhibition of Glycine Decarboxylase

Research output: Contribution to journalArticlepeer-review

156 Citations (Scopus)


A cytotoxic product of lipid peroxidation, 4-hydroxy-2-nonenal (HNE), rapidly inhibited glycine, malate/pyruvate, and 2-oxoglutarate-dependent O-2 consumption by pea leaf mitochondria. Dose- and time-dependence of inhibition showed that glycine oxidation was the most severely affected with a K-0.5 of 30 mum. Several mitochondrial proteins containing lipoic acid moieties differentially lost their reactivity to a lipoic acid antibody following HNE treatment. The most dramatic loss of antigenicity was seen with the 17-kDa glycine decarboxylase complex (GDC) H-protein, which was correlated with the loss of glycine-dependent O-2 consumption. Paraquat treatment of pea seedlings induced lipid peroxidation, which resulted in the rapid loss of glycine-dependent respiration and loss of H-protein reactivity with lipoic acid antibodies. Pea plants exposed to chilling and water deficit responded similarly. In contrast, the damage to other lipoic acid-containing mitochondrial enzymes was minor under these conditions. The implication of the acute sensitivity of glycine decarboxylase complex H-protein to lipid peroxidation products is discussed in the context of photorespiration and potential repair mechanisms in plant mitochondria.
Original languageEnglish
Pages (from-to)42663-442668
JournalJournal of Biological Chemistry
Issue number45
Publication statusPublished - 2002


Dive into the research topics of 'Environmental Stress Causes Oxidative Damage to Plant Mitochondria Leading to Inhibition of Glycine Decarboxylase'. Together they form a unique fingerprint.

Cite this