taurochenodeoxycholic-acid and titanium-dioxide

taurochenodeoxycholic-acid has been researched along with titanium-dioxide* in 1 studies

Other Studies

1 other study(ies) available for taurochenodeoxycholic-acid and titanium-dioxide

Article	Year
Titanium Dioxide Nanoparticles Induce Endoplasmic Reticulum Stress-Mediated Autophagic Cell Death via Mitochondria-Associated Endoplasmic Reticulum Membrane Disruption in Normal Lung Cells. PloS one, 2015, Volume: 10, Issue:6 Nanomaterials are used in diverse fields including food, cosmetic, and medical industries. Titanium dioxide nanoparticles (TiO2-NP) are widely used, but their effects on biological systems and mechanism of toxicity have not been elucidated fully. Here, we report the toxicological mechanism of TiO2-NP in cell organelles. Human bronchial epithelial cells (16HBE14o-) were exposed to 50 and 100 μg/mL TiO2-NP for 24 and 48 h. Our results showed that TiO2-NP induced endoplasmic reticulum (ER) stress in the cells and disrupted the mitochondria-associated endoplasmic reticulum membranes (MAMs) and calcium ion balance, thereby increasing autophagy. In contrast, an inhibitor of ER stress, tauroursodeoxycholic acid (TUDCA), mitigated the cellular toxic response, suggesting that TiO2-NP promoted toxicity via ER stress. This novel mechanism of TiO2-NP toxicity in human bronchial epithelial cells suggests that further exhaustive research on the harmful effects of these nanoparticles in relevant organisms is needed for their safe application. Topics: Autophagy; Calcium; Cells, Cultured; Endoplasmic Reticulum; Endoplasmic Reticulum Stress; Epithelial Cells; Homeostasis; Humans; Intracellular Membranes; Lung; Mitochondria; Nanoparticles; Reactive Oxygen Species; Taurochenodeoxycholic Acid; Titanium	2015

Article

Year

Titanium Dioxide Nanoparticles Induce Endoplasmic Reticulum Stress-Mediated Autophagic Cell Death via Mitochondria-Associated Endoplasmic Reticulum Membrane Disruption in Normal Lung Cells.

PloS one, 2015, Volume: 10, Issue:6

Nanomaterials are used in diverse fields including food, cosmetic, and medical industries. Titanium dioxide nanoparticles (TiO2-NP) are widely used, but their effects on biological systems and mechanism of toxicity have not been elucidated fully. Here, we report the toxicological mechanism of TiO2-NP in cell organelles. Human bronchial epithelial cells (16HBE14o-) were exposed to 50 and 100 μg/mL TiO2-NP for 24 and 48 h. Our results showed that TiO2-NP induced endoplasmic reticulum (ER) stress in the cells and disrupted the mitochondria-associated endoplasmic reticulum membranes (MAMs) and calcium ion balance, thereby increasing autophagy. In contrast, an inhibitor of ER stress, tauroursodeoxycholic acid (TUDCA), mitigated the cellular toxic response, suggesting that TiO2-NP promoted toxicity via ER stress. This novel mechanism of TiO2-NP toxicity in human bronchial epithelial cells suggests that further exhaustive research on the harmful effects of these nanoparticles in relevant organisms is needed for their safe application.

Topics: Autophagy; Calcium; Cells, Cultured; Endoplasmic Reticulum; Endoplasmic Reticulum Stress; Epithelial Cells; Homeostasis; Humans; Intracellular Membranes; Lung; Mitochondria; Nanoparticles; Reactive Oxygen Species; Taurochenodeoxycholic Acid; Titanium

2015