Origin of cadmium-induced reactive oxygen species production: mitochondrial electron transfer versus plasma membrane NADPH oxidase
Article first published online: 5 JUN 2008
© The Authors (2008). Journal compilation © New Phytologist (2008)
Volume 179, Issue 3, pages 687–699, August 2008
How to Cite
Heyno, E., Klose, C. and Krieger-Liszkay, A. (2008), Origin of cadmium-induced reactive oxygen species production: mitochondrial electron transfer versus plasma membrane NADPH oxidase. New Phytologist, 179: 687–699. doi: 10.1111/j.1469-8137.2008.02512.x
- Issue published online: 15 JUL 2008
- Article first published online: 5 JUN 2008
- Received: 25 March 2008 Accepted: 16 April 2008
- cadmium (Cd);
- calcium (Ca);
- mitochondrial electron transport chain;
- NADPH oxidase;
- plasma membrane;
- reactive oxygen species (ROS)
- • Cadmium (Cd2+) is an environmental pollutant that causes increased reactive oxygen species (ROS) production. To determine the site of ROS production, the effect of Cd2+ on ROS production was studied in isolated soybean (Glycine max) plasma membranes, potato (Solanum tuberosum) tuber mitochondria and roots of intact seedlings of soybean or cucumber (Cucumis sativus).
- • The effects of Cd2+ on the kinetics of superoxide (), hydrogen peroxide (H2O2) and hydroxyl radical (•OH) generation were followed using absorption, fluorescence and spin-trapping electron paramagnetic resonance spectroscopy.
- • In isolated plasma membranes, Cd2+ inhibited production. This inhibition was reversed by calcium (Ca2+) and magnesium (Mg2+). In isolated mitochondria, Cd2+ increased and H2O2 production. In intact roots, Cd2+ stimulated H2O2 production whereas it inhibited and •OH production in a Ca2+-reversible manner.
- • Cd2+ can be used to distinguish between ROS originating from mitochondria and from the plasma membrane. This is achieved by measuring different ROS individually. The immediate (≤ 1 h) consequence of exposure to Cd2+ in vivo is stimulation of ROS production in the mitochondrial electron transfer chain and inhibition of NADPH oxidase activity in the plasma membrane.