PCDD/Fs-induced oxidative damage and antioxidant system responses in tobacco cell suspension cultures |
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Authors: | Zhang Baoqin Zhang Haijun Jin Jing Ni Yuwen Chen Jiping |
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Affiliation: | a Dalian Institute of Chemical Physics, Chinese Academy of Sciences, 457 Zhongshan Road, Dalian 116023, China b Graduate University of Chinese Academy of Sciences, Beijing 100049, China |
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Abstract: | Polychlorinated dibenzo-p-dioxins and polychlorinated dibenzofurans (PCDD/Fs) are ubiquitous contaminants and can be considerably accumulated by natural plants. In order to elucidate the biochemical and physiological responses of plant to PCDD/Fs, tobacco Bright Yellow-2 (BY-2) cells were selected as model plant and treated with time- and concentration-dependent PCDD/Fs. The toxic effect and oxidative stress caused by PCDD/Fs were evident, which could be indicted by the reduction in fresh mass, the increase in malondialdehyde (MDA) content, and the damage of tobacco cell ultrastructure. PCDD/Fs tolerance was correlated with changes in antioxidant system and hormones of tobacco cells. Superoxide dismutase (SOD) and peroxidase (POD) exhibited peak enzyme activities at the PCDD/Fs concentration of 1000 ng WHO98-TEQ g−1 fresh weight. Glutathione reductase (GR) enzyme activity increased monotonically at high level PCDD/Fs, but the activity of catalase (CAT) was only slightly affected at all treatment. Meanwhile, the exposure to PCDD/Fs resulted in the changes of hormones content. With the increase of exposure concentration of PCDD/Fs, the levels of indole-3-acetic acid (IAA) and abscisic acid (ABA) increased, whereas the concentration of jasmonates (JAs) decreased. The above results suggest that tobacco cells had the ability to cope with the oxidative stress induced by low concentration of PCDD/Fs through increasing the activities of antioxidant enzymes and alternating plant hormones levels. However, oxidative stress and toxicity would burst out when plant cells were exposed to the high levels of PCDD/Fs. |
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Keywords: | PCDD/Fs, polychlorinated dibenzo-p-dioxins and dibenzofurans BY-2, Bright Yellow-2 MDA, malondialdehyde AhR, aryl hydrocarbon receptor ROIs, reactive oxygen intermediates SOD, superoxide dismutase CAT, catalase GR, glutathione reductase POD, peroxidase GPX, glutathione peroxidase IAA, indole-3-acetic acid ABA, abscisic acid JA, jasmonates SA, salicylic acid TEM, transmission electron microscopy TEQ, toxicity equivalent EDTA, ethylenediaminetetraacetic acid fw, fresh weight SIM, selected-ion monitoring EROD, specific eth-oxyresorufin O-deethylase LSD, least-significant-differences |
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