Role of surface charge and oxidative stress in cytotoxicity and genotoxicity of graphene oxide towards human lung fibroblast cells

2013 ◽  
Vol 33 (10) ◽  
pp. 1156-1164 ◽  
Author(s):  
Anxin Wang ◽  
Kefeng Pu ◽  
Bing Dong ◽  
Yang Liu ◽  
Liming Zhang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Graphene Oxide ◽  
Surface Charge ◽  
Human Lung ◽  
Lung Fibroblast ◽  
Fibroblast Cells ◽  
Human Lung Fibroblast ◽  
And Oxidative Stress

Hormetic effects of noncoplanar PCB exposed to human lung fibroblast cells (HELF) and possible role of oxidative stress

2014 ◽  
Vol 30 (12) ◽  
pp. 1385-1392 ◽  
Author(s):  
Muhammad Zaffar Hashmi ◽  
Kiran Yasmin Khan ◽  
Jinxing Hu ◽  
Naveedullah ◽  
Xiaomei Su ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Human Lung ◽  
Lung Fibroblast ◽  
Fibroblast Cells ◽  
Human Lung Fibroblast

Antioxidant effect of homogenetisic acid on hydrogen peroxide induced oxidative stress in human lung fibroblast cells

2005 ◽  
Vol 10 (6) ◽  
pp. 556-563 ◽  
Author(s):  
Kyoung Ah Kang ◽  
Sungwook Chae ◽  
Kyung Hwa Lee ◽  
Rui Zhang ◽  
Myung Sun Jung ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Hydrogen Peroxide ◽  
Human Lung ◽  
Antioxidant Effect ◽  
Lung Fibroblast ◽  
Fibroblast Cells ◽  
Human Lung Fibroblast

Presence of nanosilica (E551) in commercial food products: TNF-mediated oxidative stress and altered cell cycle progression in human lung fibroblast cells

2014 ◽  
Vol 30 (2) ◽  
pp. 89-100 ◽  
Author(s):  
Jegan Athinarayanan ◽  
Vaiyapuri Subbarayan Periasamy ◽  
Mohammed A. Alsaif ◽  
Abdulrahman A. Al-Warthan ◽  
Ali A. Alshatwi
Keyword(s):  
Oxidative Stress ◽  
Cell Cycle ◽  
Cell Cycle Progression ◽  
Human Lung ◽  
Food Products ◽  
Lung Fibroblast ◽  
Fibroblast Cells ◽  
Cycle Progression ◽  
Human Lung Fibroblast ◽  
Altered Cell

Dynamic protein hydrogels with reversibly tunable stiffness regulate human lung fibroblast spreading reversibly

2019 ◽  
Vol 55 (36) ◽  
pp. 5235-5238 ◽  
Author(s):  
Linglan Fu ◽  
Amanda Haage ◽  
Na Kong ◽  
Guy Tanentzapf ◽  
Hongbin Li
Keyword(s):  
Human Lung ◽  
Lung Fibroblast ◽  
Fibroblast Cells ◽  
Human Lung Fibroblast ◽  
Protein Hydrogels ◽  
Tunable Stiffness

Fibroblast cells change their morphology reversibly in response to changes in protein hydrogel stiffness.

scholarly journals Caffeic Acid Protects Hydrogen Peroxide Induced Cell Damage in WI-38 Human Lung Fibroblast Cells

2006 ◽  
Vol 29 (9) ◽  
pp. 1820-1824 ◽  
Author(s):  
Kyoung Ah Kang ◽  
Kyoung Hwa Lee ◽  
Rui Zhang ◽  
Meijing Piao ◽  
Sungwook Chae ◽  
...  
Keyword(s):  
Hydrogen Peroxide ◽  
Caffeic Acid ◽  
Human Lung ◽  
Cell Damage ◽  
Lung Fibroblast ◽  
Fibroblast Cells ◽  
Human Lung Fibroblast

Differential induction of apoptosis by cigarette smoke extract in primary human lung fibroblast strains: implications for emphysema

2006 ◽  
Vol 291 (1) ◽  
pp. L19-L29 ◽  
Author(s):  
Carolyn J. Baglole ◽  
Seth M. Bushinsky ◽  
Tatiana M. Garcia ◽  
Aruna Kode ◽  
Irfan Rahman ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Membrane Potential ◽  
Cigarette Smoke ◽  
Tobacco Smoke ◽  
Mitochondrial Membrane ◽  
Human Lung ◽  
Cigarette Smoke Extract ◽  
Lung Fibroblast ◽  
Cigarette Smoke Exposure ◽  
Human Lung Fibroblast

Cigarette smoke is the principal cause of emphysema. Recent attention has focused on the loss of alveolar fibroblasts in the development of emphysema. Fibroblasts may become damaged by oxidative stress and undergo apoptosis as a result of cigarette smoke exposure. Not all smokers develop lung diseases associated with tobacco smoke, a fact that may reflect individual variation among human fibroblast strains. We hypothesize that fibroblasts from different human beings vary in their ability to undergo apoptosis after cigarette smoke exposure. This could account for emphysematous changes that occur in the lungs of some but not all smokers. Primary human lung fibroblast strains were exposed to cigarette smoke extract (CSE) and assessed for viability, morphological changes, and mitochondrial transmembrane potential as indicators of apoptosis. We also examined the generation of intracellular reactive oxygen species (ROS), 4-hydroxy-2-nonenal, and changes in glutathione (GSH) and glutathione disulfide (GSSG) levels. Each human lung fibroblast strain exhibited a differential sensitivity to CSE as judged by changes in mitochondrial membrane potential, viability, ROS generation, and glutathione production. Interestingly, the thiol antioxidants N-acetyl-l-cysteine and GSH eliminated CSE-induced changes in fibroblast morphology such as membrane blebbing, nuclear condensation, and cell size and prevented alterations in mitochondrial membrane potential and the generation of ROS. These findings support the concept that oxidative stress and apoptosis are responsible for fibroblast death associated with exposure to tobacco smoke. Variations in the sensitivity of fibroblasts to cigarette smoke may account for the fact that only some smokers develop emphysema.

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