Garlic diallyl disulfide and diallyl trisulfide mitigates effects of pro-oxidant induced cellular stress and has immune modulatory function in LPS-stimulated porcine epithelial cells

2017 ◽  
Vol 95 (9) ◽  
pp. 4045 ◽  
Author(s):  
N. Horn ◽  
G. Miller ◽  
K. M. Ajuwon ◽  
O. Adeola
Keyword(s):  
Epithelial Cells ◽  
Cellular Stress ◽  
Diallyl Disulfide ◽  
Diallyl Trisulfide

scholarly journals Metformin Protects against Radiation-Induced Acute Effects by Limiting Senescence of Bronchial-Epithelial Cells

2021 ◽  
Vol 22 (13) ◽  
pp. 7064
Author(s):  
Christine Hansel ◽  
Samantha Barr ◽  
Alina V. Schemann ◽  
Kirsten Lauber ◽  
Julia Hess ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Lung Tissue ◽  
Cellular Stress ◽  
Lung Epithelial Cells ◽  
Normal Lung Tissue ◽  
Normal Lung ◽  
Metformin Treatment ◽  
Acute Effects ◽  
Lung Epithelial ◽  
Radiation Induced

Radiation-induced damage to normal lung parenchyma remains a dose-limiting factor in thorax-associated radiotherapy (RT). Severe early and late complications with lungs can increase the risk of morbidity in cancer patients after RT. Herein, senescence of lung epithelial cells following RT-induced cellular stress, or more precisely the respective altered secretory profile, the senescence-associated secretory phenotype (SASP), was suggested as a central process for the initiation and progression of pneumonitis and pulmonary fibrosis. We previously reported that abrogation of certain aspects of the secretome of senescent lung cells, in particular, signaling inhibition of the SASP-factor Ccl2/Mcp1 mediated radioprotection especially by limiting endothelial dysfunction. Here, we investigated the therapeutic potential of a combined metformin treatment to protect normal lung tissue from RT-induced senescence and associated lung injury using a preclinical mouse model of radiation-induced pneumopathy. Metformin treatment efficiently limited RT-induced senescence and SASP expression levels, thereby limiting vascular dysfunctions, namely increased vascular permeability associated with increased extravasation of circulating immune and tumor cells early after irradiation (acute effects). Complementary in vitro studies using normal lung epithelial cell lines confirmed the senescence-limiting effect of metformin following RT finally resulting in radioprotection, while fostering RT-induced cellular stress of cultured malignant epithelial cells accounting for radiosensitization. The radioprotective action of metformin for normal lung tissue without simultaneous protection or preferable radiosensitization of tumor tissue might increase tumor control probabilities and survival because higher radiation doses could be used.

scholarly journals VALIDATION AND ANALYSIS OF DIALLYL DISULFIDE AND DIALLYL TRISULFIDE IN GARLIC (ALLIUM SATIVUM L.) USING GAS CHROMATOGRAPHY

2020 ◽  
pp. 163-166
Author(s):  
HARMITA HARMITA ◽  
HERMAN SURYADI ◽  
LIDWINA DEVIANI LIKASA
Keyword(s):  
Gas Chromatography ◽  
Allium Sativum ◽  
Limit Of Detection ◽  
Diallyl Disulfide ◽  
Diallyl Trisulfide ◽  
Ionization Detector ◽  
Limit Of Quantification ◽  
Flame Ionization ◽  
Precision Limit ◽  
Optimized Conditions

Objective: The purpose of this research was to optimize and validate a method for measuring the levels of diallyl disulfide (DADS) and diallyl trisulfide(DATS) in garlic and single clove garlic.Methods: The analysis was performed using gas chromatography (GC) equipped with an HP-1 column and a flame ionization detector. The initialcolumn temperature was set at 140°C and increased at 1°C/min to 180°C. The injector and detector temperatures were set to 200°C, the carrier gasflow rate was 0.80 mL/min, and the injection volume was 1.0 μL. The optimized conditions of analysis were then validated which included selectivity,linearity, accuracy, precision, limit of detection (LOD), and limit of quantification (LOQ).Results: Using the validated assay and a concentration range of 0.5–20 μg/mL, the coefficient of correlation (r) for DADS was 0.9999 and the LODand LOQ for DADS were 0.3063 μg/mL and 1.0210 μg/mL, respectively. Using the validated assay and a concentration range of 0.5–20 μg/mL, thecoefficient of correlation for DATS was 0.9999 and the LOD and LOQ for DATS were 0.1986 μg/mL and 0.6621 μg/mL, respectively. The percentage ofrecovery was in the range of 98.05–101.76% and coefficient of variation ≤ 2%.Conclusion: This GC method accurately measures the levels of DADS and DATS in garlic.

scholarly journals Screening of Cellular Stress Responses Induced by Ambient Aerosol Ultrafine Particle Fraction PM0.5 in A549 Cells

2019 ◽  
Vol 20 (24) ◽  
pp. 6310 ◽  
Author(s):  
Pavlína Šimečková ◽  
Soňa Marvanová ◽  
Pavel Kulich ◽  
Lucie Králiková ◽  
Jiří Neča ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Oxidative Damage ◽  
Stress Responses ◽  
Expression Profiles ◽  
Cellular Stress ◽  
A549 Cells ◽  
Lung Epithelial Cells ◽  
Particle Fraction ◽  
Gene Markers ◽  
Ambient Aerosol

Effects of airborne particles on the expression status of markers of cellular toxic stress and on the release of eicosanoids, linked with inflammation and oxidative damage, remain poorly characterized. Therefore, we proposed a set of various methodological approaches in order to address complexity of PM0.5-induced toxicity. For this purpose, we used a well-characterized model of A549 pulmonary epithelial cells exposed to a non-cytotoxic concentration of ambient aerosol particle fraction PM0.5 for 24 h. Electron microscopy confirmed accumulation of PM0.5 within A549 cells, yet, autophagy was not induced. Expression profiles of various cellular stress response genes that have been previously shown to be involved in early stress responses, namely unfolded protein response, DNA damage response, and in aryl hydrocarbon receptor (AhR) and p53 signaling, were analyzed. This analysis revealed induction of GREM1, EGR1, CYP1A1, CDK1A, PUMA, NOXA and GDF15 and suppression of SOX9 in response to PM0.5 exposure. Analysis of eicosanoids showed no oxidative damage and only a weak anti-inflammatory response. In conclusion, this study helps to identify novel gene markers, GREM1, EGR1, GDF15 and SOX9, that may represent a valuable tool for routine testing of PM0.5-induced in vitro toxicity in lung epithelial cells.

Cigarette smoke extract affects mitochondrial function in alveolar epithelial cells

2014 ◽  
Vol 307 (11) ◽  
pp. L895-L907 ◽  
Author(s):  
Korbinian Ballweg ◽  
Kathrin Mutze ◽  
Melanie Königshoff ◽  
Oliver Eickelberg ◽  
Silke Meiners
Keyword(s):  
Stress Response ◽  
Epithelial Cells ◽  
Cigarette Smoke ◽  
Cellular Stress ◽  
Cigarette Smoke Extract ◽  
Mitochondrial Fusion ◽  
Alveolar Epithelial Cells ◽  
Mitochondrial Morphology ◽  
Mild Stress ◽  
Alveolar Epithelial

Cigarette smoke is the main risk factor for chronic obstructive pulmonary disease (COPD). Exposure of cells to cigarette smoke induces an initial adaptive cellular stress response involving increased oxidative stress and induction of inflammatory signaling pathways. Exposure of mitochondria to cellular stress alters their fusion/fission dynamics. Whereas mild stress induces a prosurvival response termed stress-induced mitochondrial hyperfusion, severe stress results in mitochondrial fragmentation and mitophagy. In the present study, we analyzed the mitochondrial response to mild and nontoxic doses of cigarette smoke extract (CSE) in alveolar epithelial cells. We characterized mitochondrial morphology, expression of mitochondrial fusion and fission genes, markers of mitochondrial proteostasis, as well as mitochondrial functions such as membrane potential and oxygen consumption. Murine lung epithelial (MLE)12 and primary mouse alveolar epithelial cells revealed pronounced mitochondrial hyperfusion upon treatment with CSE, accompanied by increased expression of the mitochondrial fusion protein mitofusin 2 and increased metabolic activity. We did not observe any alterations in mitochondrial proteostasis, i.e., induction of the mitochondrial unfolded protein response or mitophagy. Therefore, our data indicate an adaptive prosurvival response of mitochondria of alveolar epithelial cells to nontoxic concentrations of CSE. A hyperfused mitochondrial network, however, renders the cell more vulnerable to additional stress, such as sustained cigarette smoke exposure. As such, cigarette smoke-induced mitochondrial hyperfusion, although part of a beneficial adaptive stress response in the first place, may contribute to the pathogenesis of COPD.

scholarly journals Allicin and Digestive System Cancers: From Chemical Structure to Its Therapeutic Opportunities

2021 ◽  
Vol 11 ◽  
Author(s):  
Mahshad Sarvizadeh ◽  
Omid Hasanpour ◽  
Zari Naderi Ghale-Noie ◽  
Samaneh Mollazadeh ◽  
Mohammad Rezaei ◽  
...  
Keyword(s):  
Chemical Structure ◽  
Digestive System ◽  
Therapeutic Potential ◽  
Diallyl Disulfide ◽  
Enzymatic Reactions ◽  
Diallyl Trisulfide ◽  
Epidemiological Evidence ◽  
Anticancer Efficacy ◽  
Skin Cancers ◽  
Gi Cancers

Digestive system cancer tumors are one of the major causes of cancer-related fatalities; the vast majority of them are colorectal or gastric malignancies. Epidemiological evidence confirmed that allium-containing food, such as garlic, reduces the risk of developing malignancies. Among all compounds in garlic, allicin has been most researched, as it contains sulfur and produces many second degradation compounds, such as sulfur dioxide, diallyl sulfide (DAS), diallyl trisulfide (DATS), and diallyl disulfide (DADS) in the presence of enzymatic reactions in gastric juice. These substances have shown anti-inflammatory, antidiabetic, antihypertensive, antifungal, antiviral, antibacterial, and anticancer efficacy, including gastrointestinal (GI) cancers, leukemia, and skin cancers. Herein, we summarize the therapeutic potential of allicin in the treatment of GI cancers.

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