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Title: DIAPHORASE-MEDICATED OXYGEN ACTIVATION AND UNCOUPLING OF MITOCHONDRIAL ELECTRON TRANSPORT BY NAPHTHAZARIN TOXINS PRODUCED BY FUSARIUM SOLANI

Author
item ROHNERT, UTE - TECH UNIV OF MUNICH
item HEISER, INGRID - TECH UNIV OF MUNICH
item NEMEC, STAN - RETIRED FROM USDA
item Baker, Robert
item OSSWALD, WOLFGANG - LMU-MUNICH
item ELSTNER, ERICH - TECH UNIV OF MUNICH

Submitted to: Journal of Plant Physiology
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 4/9/1998
Publication Date: N/A
Citation: N/A

Interpretive Summary: Fusarium solani, a pathogen of citrus, peas and tomatoes, produces a group of toxic compounds known as naphthazarins. Previous work had isolated a number of these compounds from F. solani cultures derived from citrus roots. Several of these compounds were shown to produce reactive oxygen radicals, particularly a strongly reactive -OH radical, which could initiate lipid peroxidation of membranes. This could account for some of the disease symptoms, such as wilting, stem collapse and leaf withering seen in plants infected with this fungus. These compounds also acted as uncouplers of the mitochondrial electron transport chain, thus interfering with the energy metabolism of cells.

Technical Abstract: Naphthazarin toxins such as dihydrofusarubin, marticin, isomarticin and methyljavanicin are produced by Fusarium solani, a pathogen for citrus, peas and tomatoes. Similar to other p-quinones such as several members of the anthraquinone- or 1,4-naphthoquinone-families, dihydrofusarubin, marticin and isomarticin were reductively activated by diaphorases at the expense of NAD(P)H. Upon autoxidation, the reduced compounds activated oxygen forming superoxide and hydrogen peroxide. Finally a strong oxidant similar to OH -radial was produced in an iron-dependent reaction. The Fusarium solani toxins did not show redox-coupling with isolated mitochondria neither at the expense of NADH nor of succinate. However, the naphthazarin derivates marticin, isomarticin and methyljavanicin, but not dihydrofusarubin, acted as uncouplers of the mitochondrial electron transport chain.