Cadmium nitrate-induced neuronal apoptosis is protected by N-acetyl-l-cysteine via reducing reactive oxygen species generation and mitochondria dysfunction
| Autor: | Chen-Yu Chian, Ya-Lan Chang, Chien-Ying Lee, Meng-Liang Lin, Yu-Hsiang Kuan, Ming-Ling Yang, Shiuan-Shinn Lee, Rosa Huang-Liu, Chun-Jung Chen, Ping-Kun Tsai, Chia-Hui Chen, Chun-Hung Su, Wen-Ying Chen, Yung-Chyuan Ho |
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| Rok vydání: | 2018 |
| Předmět: |
inorganic chemicals
0301 basic medicine Programmed cell death Necrosis Cell Survival Apoptosis Mitochondrion Rats Sprague-Dawley Mice 03 medical and health sciences 0302 clinical medicine Annexin Cell Line Tumor Cadmium Compounds medicine Animals Caspase Membrane Potential Mitochondrial Neurons Pharmacology chemistry.chemical_classification Reactive oxygen species Nitrates Cell Death biology Neurodegeneration General Medicine medicine.disease Molecular biology Acetylcysteine Mitochondria Rats 030104 developmental biology chemistry Caspases biology.protein medicine.symptom Reactive Oxygen Species 030217 neurology & neurosurgery Signal Transduction |
| Zdroj: | Biomedicine & Pharmacotherapy. 108:448-456 |
| ISSN: | 0753-3322 |
| Popis: | Cigarette smoking is a well-established risk factor for various diseases, such as cardiovascular diseases, neurodegeneration, and cancer. Cadmium nitrate (Cd(NO3)2) is one of the major products from the cigarette smoke. Up to now, no supporting evidence on Cd(NO3)2-induced apoptosis and its related working mechanism in neurons has been found. In present study, the mode of cell death, caspase activities, reactive oxygen species (ROS) generation, and mitochondrial dysfunction in N2a cells, which are neuron-like cells, were assessed by Annexin V-FITC and PI assays, caspase fluorometric assay, DCFH-DA fluorescence assay, and JC-1 fluorescence assay respectively. The results showed that not only Cd(NO3)2 induced apoptosis and necrosis but also the activities of caspase-3 and -9 expressed in a concentration-dependent manner. In addition, Cd(NO3)2 also induced both mitochondrial dysfunction and ROS generation in a concentration-dependent manner. All these indicated that in N2a cells parallel trends could be observed in apoptosis, caspase-3 and -9 activities, mitochondrial dysfunction, and ROS generation when induced by Cd(NO3)2. Furthermore, Cd(NO3)2-induced apoptosis, caspases activities, mitochondrial dysfunction, and ROS generation were reduced by N-acetyl-l-cysteine (NAC). These results indicated that Cd(NO3)2-induced neuronal apoptosis was reduced by NAC via intrinsic apoptotic caspase cascade activities and their up-stream factors, including mitochondrial dysfunction and ROS generation. |
| Databáze: | OpenAIRE |
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