Cadmium nitrate-induced neuronal apoptosis is protected by N-acetyl-l-cysteine via reducing reactive oxygen species generation and mitochondria dysfunction

Publication date: December 2018Source: Biomedicine & Pharmacotherapy, Volume 108Author(s): Chien-Ying Lee, Chun-Hung Su, Ping-Kun Tsai, Ming-Ling Yang, Yung-Chyuan Ho, Shiuan-Shinn Lee, Chia-Hui Chen, Wen-Ying Chen, Meng-Liang Lin, Chun-Jung Chen, Chen-Yu Chian, Rosa Huang-Liu, Ya-Lan Chang, Yu-Hsiang KuanAbstractCigarette 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, casp...
Source: Biomedicine and Pharmacotherapy - Category: Drugs & Pharmacology Source Type: research