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The relationship between potassium deficiency and the antioxidative defense system has received little study. The aim of this work was to study the induction of oxidative stress in response to K(+) deficiency and the putative role of antioxidants. The tomato plants were grown in hydroponic systems to determine the role of reactive oxygen species (ROS) in the root response to potassium deprivation. Parameters of oxidative stress (malondialdehyde and hydrogen peroxide (H(2)O(2)) concentration), activities of antioxidant enzymes (superoxide dismutase (SOD), catalase (CAT), ascorbate peroxidase (APX), dehydroascorbate reductase (DHAR) and glutathione reductase (GR)) and antioxidant molecules (ascorbate (ASC) and glutathione) were investigated. H(2)O(2) was subcellularly located by laser confocal microscopy after potassium starvation in roots. During the first 24h, H(2)O(2) induced the cascade of the cellular response to low potassium, and ROS accumulation was located mainly in epidermal cells in the elongation zone and meristematic cells of the root tip and the epidermal cells of the mature zones of potassium starved roots. The activity of the antioxidative enzymes SOD, peroxidase and APX in potassium deprivation significantly increased, whereas CAT and DHAR activity was significantly depressed in the potassium starvation treatment compared to controls. GR did not show significant differences between control and potassium starvation treatments. Based on these results, we put forward the hypothesis that antioxidant molecule accumulations probably scavenge H(2)O(2) and might be regenerated by the ASC-glutathione cycle enzymes, such as DHAR and GR.
Department of Stress Biology and Plant Pathology, CEBAS-CSIC, Campus de Espinardo, P.O. Box 164, 30100 Espinardo-Murcia, Spain.
This article was published in the following journal.
Name: Journal of plant physiology
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A disturbance in the prooxidant-antioxidant balance in favor of the former, leading to potential damage. Indicators of oxidative stress include damaged DNA bases, protein oxidation products, and lipid peroxidation products (Sies, Oxidative Stress, 1991, pxv-xvi).
A condition due to decreased dietary intake of potassium, as in starvation or failure to administer in intravenous solutions, or to gastrointestinal loss in diarrhea, chronic laxative abuse, vomiting, gastric suction, or bowel diversion. Severe potassium deficiency may produce muscular weakness and lead to paralysis and respiratory failure. Muscular malfunction may result in hypoventilation, paralytic ileus, hypotension, muscle twitches, tetany, and rhabomyolysis. Nephropathy from potassium deficit impairs the concentrating mechanism, producing polyuria and decreased maximal urinary concentrating ability with secondary polydipsia. (Merck Manual, 16th ed)
Permanganic acid (HMnO4), potassium salt. A highly oxidative, water-soluble compound with purple crystals, and a sweet taste. (From McGraw-Hill Dictionary of Scientific and Technical Information, 4th ed)
The appearance of carbonyl groups (such as aldehyde or ketone groups) in PROTEINS as the result of several oxidative modification reactions. It is a standard marker for OXIDATIVE STRESS. Carbonylated proteins tend to be more hydrophobic and resistant to proteolysis.
A direct-acting oxidative stress-inducing agent used to examine the effects of oxidant stress on Ca(2+)-dependent signal transduction in vascular endothelial cells. It is also used as a catalyst in polymerization reactions and to introduce peroxy groups into organic molecules.
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