Cytotoxic and genotoxic evaluation and the toxicological mechanism of uranium in Vicia faba root

• Published in: Environmental and experimental botany Vol. 179; p. 104227
• Main Authors: Chen, Xi, Wu, Guo, Ma, Qiong, Lai, Jin-long, Luo, Xue-gang, Ji, Xiao-hui
• Format: Journal Article
• Language: English
• Published: Elsevier B.V 01.11.2020
• Subjects: Cytotoxicity; Genotoxicity; Toxicological mechanism; Uranium; Vicia faba; Cytotoxicity; Uranium; Vicia faba; Genotoxicity; Toxicological mechanism
• ISSN: 0098-8472; 1873-7307
• DOI: 10.1016/j.envexpbot.2020.104227

•Uranium induced apoptosis of root border cells in Vicia faba.•Uranium exposure damaged DNA and blocked the mitosis.•Uranium interfered with the antioxidant enzyme system and DNA repair system. This study revealed the cytotoxicity, genotoxicity and toxicity mechanism of uranium (U) in plants. The cytotoxic effect of U was evaluated by detecting the survival status of root border cells; the genotoxic effect was evaluated by micronuclear experiments; and the toxicity mechanism of U to plants was primarily revealed by combining with transcriptome. Results showed that after U exposure, the proportion of late apoptotic cells and dead cells was significantly higher than the control, indicating that U could induce the apoptosis or necrosis of root border cells. The micronucleus rate increased dramatically after U exposure, reaching a maximum of 4.89 times the control, whereas the mitotic index decreased significantly, reaching a minimum of 26.00% of the control. Moreover, the activities of superoxide dismutase and peroxidase decreased, triggering severe oxidative stress. Combined with the transcriptome data, this study showed that U interfered with the expression of genes related to antioxidant enzymes, the cell cycle and the DNA repair system. In conclusion, U strongly terminated the root border cells and blocked the mitosis, therefore inhibiting the growth of the Vicia faba root. It also caused DNA damage by interfering with the antioxidant enzymes to trigger oxidative stress and prevented DNA self-repair by interfering with the DNA repair system.