Journal
JOURNAL OF BIOMEDICAL MATERIALS RESEARCH PART A
Volume 104, Issue 1, Pages 124-135Publisher
WILEY
DOI: 10.1002/jbm.a.35548
Keywords
titanium dioxide nanoparticles; primary cultured Sertoli cells; apoptosis; mitochondrial stress; endoplasmic reticulum stress
Funding
- National Natural Science Foundation of China [81473007, 81273036, 30901218]
- Bringing New Ideas Foundation of Huaiyin Normal University
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Titanium dioxide nanoparticles (TiO2 NPs), as largest production and use of nanomaterials, have been demonstrated to have a potential toxicity on reproductive system. However, the mechanism underlying male reproductive toxicity of TiO2 NPs remains limited. Thus, our study was designed to examine the cellular viability, apoptosis, oxidative stress, antioxidant capacity, and expression of apoptotic cytokines in primary cultured Sertoli cells isolated from mice under TiO2 NPs exposure. Results showed that TiO2 NPs exposure from 5 to 30 g/mL resulted in reduction of cell viability, lactate dehydrogenase release, and induction of apoptosis or death on Sertoli cells. TiO2 NPs could migrate to Sertoli cells, which induced mitochondria-mediated or endoplasmic-reticulum-mediated apoptotic changes including elevation in reactive oxygen species (ROS) generation and reductions in superoxide dismutase, catalase, and glutathione peroxidase activities, decreases in mitochondrial membrane potential (m), and releases of cytochrome c into the cytosol. In addition, upregulation of cytochrome c, Bax, caspase-3, glucose-regulated protein 78, and C/EBP homologous protein and caspase-12 protein expression, and downregulation of bcl-2 protein expression in primary cultured Sertoli cells induced by TiO2 NPs treatment. All of the results suggested that ROS generation may play a critical role in the initiation of TiO2 NPs-induced apoptosis by mediation of the disruption of m, the cytochrome c release, and further the activation of caspase cascade and unfolded protein response signaling pathway. (c) 2015 Wiley Periodicals, Inc.
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