Phenotypical, physiological and biochemical analyses provide insight into selenium-induced phytotoxicity in rice plants

• Published in: Chemosphere (Oxford) Vol. 178; pp. 212 - 223
• Main Authors: Mostofa, Mohammad Golam, Hossain, Mohammad Anwar, Siddiqui, Md. Nurealam, Fujita, Masayuki, Tran, Lam-Son Phan
• Format: Journal Article
• Language: English
• Published: England Elsevier Ltd 01.07.2017
• Subjects: Antioxidants - metabolism; Biomarkers - metabolism; Biomass; Glutathione - metabolism; Lipid Peroxidation - drug effects; Oryza - drug effects; Oryza - growth & development; Oryza - metabolism; Osmotic Pressure - drug effects; Oxidative metabolism; Oxidative Stress - drug effects; Physiological and biochemical mechanisms; Phytotoxic effects; Plant Structures - chemistry; Proline - metabolism; Selenium - analysis; Selenium - toxicity; Selenium homeostasis; Phytotoxic effects; Oxidative metabolism; Physiological and biochemical mechanisms; Selenium homeostasis
• ISSN: 0045-6535; 1879-1298
• DOI: 10.1016/j.chemosphere.2017.03.046

The present study investigated the phenotypical, physiological and biochemical changes of rice plants exposed to high selenium (Se) concentrations to gain an insight into Se-induced phytotoxicity. Results showed that exposure of rice plants to excessive Se resulted in growth retardation and biomass reduction in connection with the decreased levels of chlorophyll, carotenoids and soluble proteins. The reduced water status and an associated increase in sugar and proline levels indicated Se-induced osmotic stress in rice plants. Measurements of Se contents in roots, leaf sheaths and leaves revealed that Se was highly accumulated in leaves followed by leaf sheaths and roots. Se also potentiated its toxicity by impairing oxidative metabolism, as evidenced by enhanced accumulation of hydrogen peroxide, superoxide and lipid peroxidation product. Se toxicity also displayed a desynchronized antioxidant system by elevating the level of glutathione and the activities of superoxide dismutase, glutathione-S-transferase and glutathione peroxidase, whereas decreasing the level of ascorbic acid and the activities of catalase, glutathione reductase and dehydroascorbate reductase. Furthermore, Se triggered methylglyoxal toxicity by inhibiting the activities of glyoxalases I and II, particularly at higher concentrations of Se. Collectively, our results suggest that excessive Se caused phytotoxic effects on rice plants by inducing chlorosis, reducing sugar, protein and antioxidant contents, and exacerbating oxidative stress and methylglyoxal toxicity. Accumulation levels of Se, proline and glutathione could be considered as efficient biomarkers to indicate degrees of Se-induced phytotoxicity in rice, and perhaps in other crops. •Se-induced phytotoxicity was investigated on hydroponically grown rice plants.•Se was highly accumulated in leaves followed by leaf sheaths and roots.•Se-phytotoxicity in rice attributed to Se-induced reduction of growth and biomass.•Se-induced oxidative stress linked to impaired ROS- and MG-detoxification systems.•Pro and GSH could be used as biomarkers for detecting Se toxicity in rice.