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Cadmium toxicity is reduced by nitric oxide in rice leaves

Cadmium toxicity is reduced by nitric oxide in rice leaves We evaluate the protective effect of nitric oxide (NO) against Cadmium (Cd) toxicity in rice leaves. Cd toxicity of rice leaves was determined by the decrease of chlorophyll and protein contents. CdCl2 treatment resulted in (1) increase in Cd content, (2) induction of Cd toxicity, (3) increase in H2O2 and malondialdehyde (MDA) contents, (4) decrease in reduced form glutathione (GSH) and ascorbic acid (ASC) contents, and (5) increase in the specific activities of antioxidant enzymes (superoxide dismutase, glutathione reductase, ascorbate peroxidase, catalase, and peroxidase). NO donors [N-tert-butyl-α-phenylnitrone, 3-morpholinosydonimine, sodium nitroprusside (SNP), and ASC + NaNO2] were effective in reducing CdCl2-induced toxicity and CdCl2-increased MDA content. SNP prevented CdCl2-induced increase in the contents of H2O2 and MDA, decrease in the contents of GSH and ASC, and increase in the specific activities of antioxidant enzymes. SNP also prevented CdCl2-induced accumulation of NH4 +, decrease in the activity of glutamine synthetase (GS), and increase in the specific activity of phenylalanine ammonia-lyase (PAL). The protective effect of SNP on CdCl2-induced toxicity, CdCl2-increased H2O2, NH4 +, and MDA contents, CdCl2-decreased GSH and ASC, CdCl2-increased specific activities of antioxidant enzymes and PAL, and CdCl2-decreased activity of GS were reversed by 2-(4-carboxy-2-phenyl)-4,4,5,5-tetramethyl-imidazoline-1-oxyl-3-oxide, a NO scavenger, suggesting that protective effect by SNP is attributable to NO released. Reduction of CdCl2-induced toxicity by NO in rice leaves is most likely mediated through its ability to scavenge active oxygen species including H2O2. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Plant Growth Regulation Springer Journals

Cadmium toxicity is reduced by nitric oxide in rice leaves

Hsu, Yi; Kao, Ching
Plant Growth Regulation , Volume 42 (3) – Sep 30, 2004
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References (52)

Publisher
Springer Journals
Copyright
Copyright © 2004 by Kluwer Academic Publishers
Subject
Life Sciences; Plant Physiology
ISSN
0167-6903
eISSN
1573-5087
DOI
10.1023/B:GROW.0000026514.98385.5c
Publisher site
See Article on Publisher Site

Abstract

We evaluate the protective effect of nitric oxide (NO) against Cadmium (Cd) toxicity in rice leaves. Cd toxicity of rice leaves was determined by the decrease of chlorophyll and protein contents. CdCl2 treatment resulted in (1) increase in Cd content, (2) induction of Cd toxicity, (3) increase in H2O2 and malondialdehyde (MDA) contents, (4) decrease in reduced form glutathione (GSH) and ascorbic acid (ASC) contents, and (5) increase in the specific activities of antioxidant enzymes (superoxide dismutase, glutathione reductase, ascorbate peroxidase, catalase, and peroxidase). NO donors [N-tert-butyl-α-phenylnitrone, 3-morpholinosydonimine, sodium nitroprusside (SNP), and ASC + NaNO2] were effective in reducing CdCl2-induced toxicity and CdCl2-increased MDA content. SNP prevented CdCl2-induced increase in the contents of H2O2 and MDA, decrease in the contents of GSH and ASC, and increase in the specific activities of antioxidant enzymes. SNP also prevented CdCl2-induced accumulation of NH4 +, decrease in the activity of glutamine synthetase (GS), and increase in the specific activity of phenylalanine ammonia-lyase (PAL). The protective effect of SNP on CdCl2-induced toxicity, CdCl2-increased H2O2, NH4 +, and MDA contents, CdCl2-decreased GSH and ASC, CdCl2-increased specific activities of antioxidant enzymes and PAL, and CdCl2-decreased activity of GS were reversed by 2-(4-carboxy-2-phenyl)-4,4,5,5-tetramethyl-imidazoline-1-oxyl-3-oxide, a NO scavenger, suggesting that protective effect by SNP is attributable to NO released. Reduction of CdCl2-induced toxicity by NO in rice leaves is most likely mediated through its ability to scavenge active oxygen species including H2O2.

Journal

Plant Growth Regulation – Springer Journals

Published: Sep 30, 2004

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