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| Calcium Inhibits Ochratoxin A (OTA) Induced Arabidopsis thaliana Toxicity |
| Yang Jun Lv1, 2,韦露450103198306212562李丽婷120103198310162928 1, 2, 2 |
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Abstract In order to enrich the toxicity and its mechanism of ochratoxin A (OTA) in plants and explore the role of calcium in OTA toxicity to plants, this research studied the effect of calcium on the toxicity induced by OTA in Arabidopsis thaliana, by the observation of morphological changes, relative leakage rate of leaves, the content of reactive oxygen species (ROS) and malondialdehyde (MDA) under treatment with exogenous Ca2+, the calcium chelator ethylenebis (oxyethylenenitrilo) tetraacetic acid (EGTA) and OTA in vitro leaves of A. thaliana. The results showed that in a certain range of concentration, under the treatment of exogenous calcium, there was no significant change in leaf morphology of A. thaliana. EGTA and OTA both led to the formation of A. thaliana leaves chlorosis and necrosis of the lesion. Ca2+ and OTA treatment together could significantly inhibit the formation of A. thaliana leaves chlorosis and necrotic lesion produced induced by OTA. EGTA treatment could aggravate those effects induced by OTA. OTA treatment increased relative leakage rate and permeability of cell membrane of A. thaliana leaves. Exogenous calcium could significantly inhibit OTA induced increase in relative leakage rate of A. thaliana leaves, 20 mmol/L Ca2+ has the strongest inhibitory effect of which the inhibition rate was 61.32%. In addition, OTA treatment brought the outbreak of ROS and the accumulation of MDA in A. thaliana leaves, and therefore caused oxidative damage. Ca2+ could effectively relieve the OTA induced A. thaliana ROS burst and reduce MDA generation; the inhibition rates were 29.7% and 71.4%, respectively. It could be concluded that OTA can induce plant toxicity in A. thaliana, calcium significantly inhibts the toxicity of OTA in A. thaliana, and plays an important role in A. thaliana's stress resistance.
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Received: 27 May 2016
Published: 07 November 2016
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Corresponding Authors:
韦露450103198306212562李丽婷120103198310162928
E-mail: xuwentao1111@sina.com
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