Cigarette Smoke-induced Oxidative Stress in Lung Epithelial Cells: in vitro Biological Effects of Smoke from a Reduced Toxicant Prototype Cigarette

2010 ◽  
Vol 49 ◽  
pp. S45
Author(s):  
Mark Taylor ◽  
Tony Carr ◽  
Natalia Cockcroft ◽  
Ian M. Fearon
Keyword(s):  
Oxidative Stress ◽  
Epithelial Cells ◽  
Cigarette Smoke ◽  
Biological Effects ◽  
Lung Epithelial Cells ◽  
Lung Epithelial

scholarly journals Lung organoids and microplastic fibers: a new exposure model for emerging contaminants

2021 ◽  
Author(s):  
Anna Winkler ◽  
Nadia Santo ◽  
Laura Madaschi ◽  
Alessandro Cherubini ◽  
Francesco Rusconi ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Epithelial Cells ◽  
Optical Microscopy ◽  
Emerging Contaminants ◽  
Human Lung ◽  
Biological Effects ◽  
Lung Epithelial Cells ◽  
Exposure Model ◽  
Lung Epithelial

AbstractBackgroundThree-dimensional (3D) structured organoids are the most advanced in vitro models for studying human health effects, but they have been applied only once to evaluate the biological effects associated with microplastic exposure. Fibers from synthetic clothes and fabrics are a major source of airborne microplastics, and their release from dryer machines is still poorly understood.ObjectivesIn this study, we aimed to establish an in vitro organoid model of human lung epithelial cells to evaluate its suitability for studying the effects of airborne microplastic contamination on humans. Furthermore, we aimed to characterize the microplastic fibers (MPFs) released in the exhaust filter of a household dryer and to test their interactions and inflammatory effects on the established lung organoids.MethodsThe polyester fibers emitted from the drying of synthetic fabrics were collected. Morphological characterization of the fibers released into the air filter was performed by optical microscopy and scanning electron microscopy (SEM)/energy dispersive x-ray spectroscopy (EDS). The organoids were exposed to various MPF concentrations (1, 10, and 50 mg L−1) and analyzed by optical microscopy, SEM, and confocal microscopy. Gene expression analysis of lung-specific genes, inflammatory cytokines, and oxidative stress-related genes was achieved by quantitative reverse transcription–polymerase chain reaction (qRT-PCR).ResultsWe successfully cultured organoids with lung-specific genes. The presence of MPFs did not inhibit organoid growth, but polarized cell growth was observed along the fibers. Moreover, the MPFs did not cause inflammation or oxidative stress. Interestingly, the MPFs were coated with a cellular layer, resulting in the inclusion of fibers in the organoid.DiscussionThis work could have potential long-term implications regarding lung epithelial cells undergoing repair. This preliminary exposure study using human lung organoids could form the basis for further research regarding the toxicological assessment of emerging contaminants such as micro- or nanoplastics.

Chlorobenzene induces oxidative stress in human lung epithelial cells in vitro

2010 ◽  
Vol 242 (1) ◽  
pp. 100-108 ◽  
Author(s):  
Ralph Feltens ◽  
Iljana Mögel ◽  
Carmen Röder-Stolinski ◽  
Jan-Christoph Simon ◽  
Gunda Herberth ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Epithelial Cells ◽  
Human Lung ◽  
Lung Epithelial Cells ◽  
Lung Epithelial ◽  
Human Lung Epithelial Cells

The role of oxidative stress in the biological responses of lung epithelial cells to cigarette smoke

Biomarkers ◽  
2009 ◽  
Vol 14 (sup1) ◽  
pp. 90-96 ◽  
Author(s):  
Stephen P. Faux ◽  
Teresa Tai ◽  
David Thorne ◽  
Yong Xu ◽  
Damien Breheny ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Epithelial Cells ◽  
Cigarette Smoke ◽  
Lung Epithelial Cells ◽  
Biological Responses ◽  
Lung Epithelial

Constitutive transgenic alpha-Klotho overexpression enhances resilience to and recovery from murine acute lung injury

2021 ◽  
Author(s):  
Joshuah M Gagan ◽  
Khoa Cao ◽  
Yu-An Zhang ◽  
Jianning Zhang ◽  
Taylor L Davidson ◽  
...  
Keyword(s):  
Acute Lung Injury ◽  
Epithelial Cells ◽  
Lung Injury ◽  
Cigarette Smoke ◽  
Lung Epithelial Cells ◽  
Lung Damage ◽  
Dna Breaks ◽  
Age Related ◽  
Lung Epithelial

Aims: Normal lungs do not express alpha-Klotho (Klotho) protein but derive cytoprotection from circulating soluble Klotho. It is unclear whether chronic supranormal Klotho levels confer additional benefit. To address this, we tested the age-related effects of Klotho overexpression on acute lung injury (ALI) and recovery. Methods: Transgenic Klotho-overexpressing (Tg-Kl) and wild-type (WT) mice (2 and 6 months old) were exposed to hyperoxia (95% O2; 72 h) then returned to normoxia (21% O2; 24 h) (Hx-R). Control mice were kept in normoxia. Renal and serum Klotho, lung histology, and bronchoalveolar lavage fluid oxidative damage markers were assessed. Effects of hyperoxia were tested in human embryonic kidney cells stably expressing Klotho. A549 lung epithelial cells transfected with Klotho cDNA or vector were exposed to cigarette smoke; lactate dehydrogenase and double-strand DNA breaks were measured. Results: Serum Klotho decreased with age. Hyperoxia suppressed renal Klotho at both ages and serum Klotho at 2-months of age. Tg-Kl mice at both ages and 2-months-old WT mice survived Hx-R; 6-months-old Tg-Kl mice showed lower lung damage than age-matched WT mice. Hyperoxia directly inhibited Klotho expression and release in vitro; Klotho transfection attenuated cigarette smoke-induced cytotoxicity and DNA double-strand breaks in lung epithelial cells. Conclusions: Young animals with chronic high baseline Klotho expression are more resistant to ALI. Chronic constitutive Klotho overexpression in older Tg-Kl animals attenuates hyperoxia-induced lung damage and improves survival and short-term recovery despite an acute reduction in serum Klotho level during injury. We conclude that chronic enhancement of Klotho expression increases resilience to ALI.

Modeling cellular metabolomic effects of oxidative stress impacts from hydrogen peroxide and cigarette smoke on human lung epithelial cells

2019 ◽  
Vol 13 (3) ◽  
pp. 036014 ◽  
Author(s):  
Mei S Yamaguchi ◽  
Mitchell M McCartney ◽  
Alexandria K Falcon ◽  
Angela L Linderholm ◽  
Susan E Ebeler ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Hydrogen Peroxide ◽  
Epithelial Cells ◽  
Cigarette Smoke ◽  
Human Lung ◽  
Lung Epithelial Cells ◽  
Lung Epithelial ◽  
Human Lung Epithelial Cells

scholarly journals A Novel Protective Mechanism for Melatonin Against Acute Lung Injury: Preserving Mitochondrial Dynamic Equilibrium of Lung Epithelial Cells Through SIRT3-Dependent Deacetylation of SOD2

2022 ◽  
Author(s):  
Li Ning ◽  
Xiong Rui ◽  
Li Guorui ◽  
Fu Tinglv ◽  
Li Donghang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Acute Lung Injury ◽  
Epithelial Cells ◽  
Lung Injury ◽  
Dynamic Equilibrium ◽  
Lung Epithelial Cells ◽  
Mitochondrial Dynamic ◽  
Lung Epithelial

Abstract Mitochondrial dynamic equilibrium of lung epithelial cells is disturbed during sepsis, which contributes to abnormal mitochondrial function and acute lung injury (ALI). Melatonin is one primary hormone secreted by the pineal gland, displaying favorable antioxidative actions in sepsis and cardiopulmonary disease. However, the potential roles and molecular basis of melatonin in lipopolysaccharide (LPS)-treated lung epithelial cells have not been explored and reported. Herein, we investigated whether melatonin could protect against sepsis-induced ALI and lipopolysaccharide (LPS)-treated lung epithelial cells through mitochondrial dynamic equilibrium as well as its possible molecular targets. Wild type and Sirt3 knockout mice were instilled with LPS intratracheally for 12 hours to construct an in vivo ALI model. And A549 lung epithelial cells were used to explore the possible roles of melatonin in vitro by incubating with small interfering RNA (siRNA) against Sirt3. To figure out the involvement of melatonin receptor, si Mtnr1b and luzindole were used in cells and mice. Melatonin pretreatment significantly inhibited pathological injury, inflammatory response, oxidative stress and apoptosis in LPS-treated lung tissues and LPS-treated lung epithelial cells. Meanwhile, melatonin also shifted the dynamic course of mitochondria from fission into fusion in LPS-treated lung epithelial cells in vivo and in vitro. However, SIRT3 inhibition abolished the protective roles of melatonin in ALI. Mechanistically, we found that melatonin increased the activity and expression of SIRT3, which further promoted the deacetylation of SOD2 at K122 and K68. More importantly, melatonin exerted pulmonary protection by activating MTNR1B but not MTNR1A in ALI. Collectively, melatonin could preserve mitochondrial dynamic equilibrium of lung epithelial cells through the deacetylation of SOD2 in a SIRT3-dependent manner, which eventually alleviated LPS-elicited injury, inflammation, oxidative stress, apoptosis. Thus, melatonin may serve as a promising candidate against ALI in the future.

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