Oxidative stress and mitochondrial dysfunctions are early events in narciclasine-induced programmed cell death in tobacco Bright Yellow-2 cells

• Published in: Physiologia plantarum Vol. 144; no. 1; pp. 48 - 58
• Main Authors: Lu, Hongxia, Wan, Qi, Wang, Huahua, Na, Xiaofan, Wang, Xiaomin, Bi, Yurong
• Format: Journal Article
• Language: English
• Published: Oxford, UK Blackwell Publishing Ltd 01.01.2012; Blackwell
• Subjects: Acetylcysteine - metabolism; Amaryllidaceae Alkaloids - pharmacology; Antioxidants - metabolism; Apoptosis - drug effects; Biological and medical sciences; Catalase - metabolism; Cells, Cultured; Fundamental and applied biological sciences. Psychology; Hydrogen Peroxide - metabolism; Mitochondria - drug effects; Mitochondria - metabolism; Mitochondria - physiology; Narcissus - chemistry; Nicotiana - drug effects; Nicotiana - growth & development; Nicotiana - metabolism; Oxidative Stress - drug effects; Phenanthridines - pharmacology; Plant Growth Regulators - metabolism; Plant physiology and development; Plant Roots - chemistry; Reactive Oxygen Species - metabolism; Signal Transduction; Oxidative stress; Mitochondria; Plant physiology; Cell death; Dysfunction; Cell; Apoptosis
• ISSN: 0031-9317; 1399-3054
• DOI: 10.1111/j.1399-3054.2011.01521.x

Narciclasine (NCS) is a plant growth inhibitor isolated from the secreted mucilage of Narcissus tazetta bulbs. It is a commonly used anticancer agent in animal systems. In this study, we provide evidence to show that NCS also acts as an agent in inducing programmed cell death (PCD) in tobacco Bright Yellow‐2 (TBY‐2) cell cultures. NCS treatment induces typical PCD‐associated morphological and biochemical changes, namely cell shrinkage, chromatin condensation and nuclear DNA degradation. To investigate possible signaling events, we analyzed the production of reactive oxygen species (ROS) and the function of mitochondria during PCD induced by NCS. A biphasic behavior burst of hydrogen peroxide (H2O2) was detected in TBY‐2 cells treated with NCS, and mitochondrial transmembrane potential (MTP) loss occurred after a slight increase. Pre‐incubation with antioxidant catalase (CAT) and N‐acetyl‐l‐cysteine (NAC) not only significantly decreased the H2O2 production but also effectively retarded the decrease of MTP and reduced the percentage of cells undergoing PCD after NCS treatment. In conclusion, our results suggest that NCS induces PCD in plant cells; the oxidative stress (accumulation of H2O2) and the MTP loss play important roles during NCS‐induced PCD.