1. Proteus mirabilis alleviates zinc toxicity by preventing oxidative stress in maize (Zea mays) plants.
- Author
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Islam F, Yasmeen T, Riaz M, Arif MS, Ali S, and Raza SH
- Subjects
- Antioxidants metabolism, DNA, Bacterial genetics, DNA, Bacterial metabolism, Molecular Sequence Data, Proteus mirabilis genetics, Proteus mirabilis isolation & purification, RNA, Ribosomal, 16S genetics, RNA, Ribosomal, 16S metabolism, Sequence Analysis, DNA, Zea mays growth & development, Zea mays metabolism, Oxidative Stress, Proteus mirabilis physiology, Soil Pollutants toxicity, Zea mays drug effects, Zea mays microbiology, Zinc toxicity
- Abstract
Plant-associated bacteria can have beneficial effects on the growth and health of their host. However, the role of plant growth promoting bacteria (PGPR), under metal stress, has not been widely investigated. The present study investigated the possible mandatory role of plant growth promoting rhizobacteria in protecting plants from zinc (Zn) toxicity. The exposure of maize plants to 50µM zinc inhibited biomass production, decreased chlorophyll, total soluble protein and strongly increased accumulation of Zn in both root and shoot. Similarly, Zn enhanced hydrogen peroxide, electrolyte leakage and lipid peroxidation as indicated by malondaldehyde accumulation. Pre-soaking with novel Zn tolerant bacterial strain Proteus mirabilis (ZK1) isolated zinc (Zn) contaminated soil, alleviated the negative effect of Zn on growth and led to a decrease in oxidative injuries caused by Zn. Furthermore, strain ZK1 significantly enhanced the activities of catalase, guaiacol peroxidase, superoxide dismutase and ascorbic acid but lowered the Proline accumulation in Zn stressed plants. The results suggested that the inoculation of Zea mays plants with P. mirabilis during an earlier growth period could be related to its plant growth promoting activities and avoidance of cumulative damage upon exposure to Zn, thus reducing the negative consequences of oxidative stress caused by heavy metal toxicity., (Copyright © 2014 Elsevier Inc. All rights reserved.)
- Published
- 2014
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