scholarly journals Investigation of Cytotoxicity, Apoptosis, and Oxidative Stress Response of Fe3O4-RGO Nanocomposites in Human Liver HepG2 cells

Materials ◽  
2020 ◽  
Vol 13 (3) ◽  
pp. 660 ◽  
Author(s):  
Maqusood Ahamed ◽  
Mohd Javed Akhtar ◽  
M. A. Majeed Khan
Keyword(s):  
Oxidative Stress ◽  
Electron Microscopy ◽  
Hepg2 Cells ◽  
Human Liver ◽  
Molecular Level ◽  
Biological Response ◽  
Cycle Arrest ◽  
Transmission Electron ◽  
Mitochondrial Membrane Potential Loss ◽  
And Oxidative Stress

Iron oxide–reduced graphene oxide (Fe3O4-RGO) nanocomposites have attracted enormous interest in the biomedical field. However, studies on biological response of Fe3O4-RGO nanocomposites at the cellular and molecular level are scarce. This study was designed to synthesize, characterize, and explore the cytotoxicity of Fe3O4-RGO nanocomposites in human liver (HepG2) cells. Potential mechanisms of cytotoxicity of Fe3O4-RGO nanocomposites were further explored through oxidative stress. Prepared samples were characterized by UV-visible spectrophotometer, X-ray diffraction, scanning electron microscopy, transmission electron microscopy, and energy dispersive spectroscopy. The results demonstrated that RGO induce dose-dependent cytotoxicity in HepG2 cells. However, Fe3O4-RGO nanocomposites were not toxic. We further noted that RGO induce apoptosis in HepG2 cells, as evidenced by mitochondrial membrane potential loss, higher caspase-3 enzyme activity, and cell cycle arrest. On the other hand, Fe3O4-RGO nanocomposites did not alter these apoptotic parameters. Moreover, we observed that RGO increases intracellular reactive oxygen species and hydrogen peroxide while decrease antioxidant glutathione. Again, Fe3O4-RGO nanocomposites did not exert oxidative stress. Altogether, we found that RGO significantly induced cytotoxicity, apoptosis and oxidative stress. However, Fe3O4-RGO nanocomposites showed good biocompatibility to HepG2 cells. This study warrants further research to investigate the biological response of Fe3O4-RGO nanocomposites at the gene and molecular level.

Effects of Amaranthus cruentus L. on aflatoxin B1- and oxidative stress-induced DNA damage in human liver (HepG2) cells

2018 ◽  
Vol 26 ◽  
pp. 42-48 ◽  
Author(s):  
Grace A. Odongo ◽  
Nina Schlotz ◽  
Susanne Baldermann ◽  
Susanne Neugart ◽  
Benard Ngwene ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Dna Damage ◽  
Aflatoxin B1 ◽  
Hepg2 Cells ◽  
Human Liver ◽  
Amaranthus Cruentus ◽  
And Oxidative Stress

1,8-Cineole promotes G0/G1 cell cycle arrest and oxidative stress-induced senescence in HepG2 cells and sensitizes cells to anti-senescence drugs

Life Sciences ◽  
2020 ◽  
Vol 243 ◽  
pp. 117271 ◽  
Author(s):  
Boris Rodenak-Kladniew ◽  
Agustina Castro ◽  
Peter Stärkel ◽  
Marianela Galle ◽  
Rosana Crespo
Keyword(s):  
Oxidative Stress ◽  
Cell Cycle ◽  
Cell Cycle Arrest ◽  
Hepg2 Cells ◽  
Cycle Arrest ◽  
G1 Cell Cycle Arrest ◽  
And Oxidative Stress

scholarly journals Mechanistic Insights into Oxidative Stress and Apoptosis Mediated by Tannic Acid in Human Liver Hepatocellular Carcinoma Cells

2019 ◽  
Vol 20 (24) ◽  
pp. 6145 ◽  
Author(s):  
Priscilla Mhlanga ◽  
Pearl O. Perumal ◽  
Anou M. Somboro ◽  
Daniel G. Amoako ◽  
Hezekiel M. Khumalo ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Hepatocellular Carcinoma ◽  
Cell Death ◽  
Dna Fragmentation ◽  
Tannic Acid ◽  
Hepg2 Cells ◽  
Human Liver ◽  
Dna Integrity ◽  
Liver Hepatocellular Carcinoma ◽  
And Oxidative Stress

The study investigated the cytotoxic effect of a natural polyphenolic compound Tannic acid (TA) on human liver hepatocellular carcinoma (HepG2) cells and elucidated the possible mechanisms that lead to apoptosis and oxidative stress HepG2 cell. The HepG2 cells were treated with TA for 24 h and various assays were conducted to determine whether TA could induce cell death and oxidative stress. The cell viability assay was used to determine the half maximal inhibitory concentration (IC50), caspase activity and cellular ATP were determined by luminometry. Microscopy was employed to determine deoxyribonucleic acid (DNA) integrity, while thiobarbituric acid (TBARS) and nitric oxide synthase (NOS) assays were used to elucidate cellular reactive oxygen species (ROS) and reactive nitrogen species (RNS), respectively. Western blotting was used to confirm protein expression. The results revealed that tannic acid induced caspase activation and increased the presence of cellular ROS and RNS, while downregulating antioxidant expression. Tannic acid also showed increased cell death and increased DNA fragmentation. In conclusion, TA was able to induce apoptosis by DNA fragmentation via caspase-dependent and caspase-independent mechanism. It was also able to induce oxidative stress, consequently contributing to cell death.

scholarly journals Autophagy attenuates high glucose-induced oxidative injury to lens epithelial cells

2020 ◽  
Vol 40 (4) ◽  
Author(s):  
Xiaomin Liu ◽  
Xiaowen Zhao ◽  
Rong Cheng ◽  
Yusen Huang
Keyword(s):  
Oxidative Stress ◽  
Electron Microscopy ◽  
Transmission Electron Microscopy ◽  
Epithelial Cells ◽  
High Glucose ◽  
Lens Epithelial Cells ◽  
Ros Generation ◽  
Diabetic Mice ◽  
Transmission Electron ◽  
And Oxidative Stress

Abstract Purpose: Autophagic dysfunction and abnormal oxidative stress are associated with cataract. The purpose of the present study was to investigate the changes of cellular autophagy and oxidative stress and their association in lens epithelial cells (LECs) upon exposure to high glucose. Methods: Autophagy and oxidative stress-related changes were detected in streptozotocin-induced Type 1 diabetic mice and normal mouse LECs incubated in high glucose conditions. Rapamycin at a concentration of 100 nm/l or 50 μM chloroquine was combined for analysis of the relationship between autophagy and oxidative stress. The morphology of LECs during autophagy was observed by transmission electron microscopy. The expressions of autophagy markers (LC3B and p62) were identified, as well as the key factors of oxidative stress (SOD2 and CAT) and mitochondrial reactive oxygen species (ROS) generation. Results: Transmission electron microscopy indicated an altered autophagy activity in diabetic mouse lens tissues with larger autophagosomes and multiple mitochondria. Regarding the expressions, LC3B was elevated, p62 was decreased first and then increased, and SOD2 and CAT were increased before a decrease during 4 months of follow-up in diabetic mice and 72 h of culture under high glucose for mouse LECs. Furthermore, rapamycin promoted the expressions of autophagy markers but alleviated those of oxidative stress markers, whereas chloroquine antagonized autophagy but enhanced oxidative stress by elevating ROS generation in LECs exposed to high glucose. Conclusions: The changes in autophagy and oxidative stress were fluctuating in the mouse LECs under constant high glucose conditions. Autophagy might attenuate high glucose-induced oxidative injury to LECs.

Hydrogen peroxide and quercetin induced changes on cell viability, apoptosis and oxidative stress in HepG2 cells

2020 ◽  
Vol 01 ◽  
Author(s):  
Ayşe Mine Yılmaz ◽  
Gökhan Biçim ◽  
Kübra Toprak ◽  
Betül Karademir Yılmaz ◽  
Irina Milisav ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cell Cycle ◽  
Hydrogen Peroxide ◽  
Cell Viability ◽  
Hepg2 Cells ◽  
Proteasome Activity ◽  
Cell Cycle Phases ◽  
Induced Changes ◽  
And Oxidative Stress ◽  
Quercetin Treatment

Background: Different cellular responses influence the progress of cancer. In this study, we have investigated the effect of hydrogen peroxide and quercetin induced changes on cell viability, apoptosis and oxidative stress in human hepatocellular carcinoma (HepG2) cells. Methods: The effects of hydrogen peroxide and quercetin on cell viability, cell cycle phases and oxidative stress related cellular changes were investigated. Cell viability was assessed by WST-1 assay. Apoptosis rate, cell cycle phase changes and oxidative stress were measured by flow cytometry. Protein expressions of p21, p27, p53, NF-Kβ-p50 and proteasome activity were determined by Western blot and fluorometry, respectively. Results: Hydrogen peroxide and quercetin treatment resulted in decreased cell viability and increased apoptosis in HepG2 cells. Proteasome activity was increased by hydrogen peroxide but decreased by quercetin treatment. Conclusion: Both agents resulted in decreased p53 protein expression and increased cell death by different mechanisms regarding proteostasis and cell cycle phases.

scholarly journals Correlative Microscopy to Localize and Characterize Iron Deposition in Alzheimer’s Disease

2020 ◽  
Vol 4 (1) ◽  
pp. 525-536
Author(s):  
Steven J. Madsen ◽  
Phillip S. DiGiacomo ◽  
Yitian Zeng ◽  
Maged Goubran ◽  
Yuanxin Chen ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Electron Microscope ◽  
Oxidation State ◽  
Transmission Electron Microscope ◽  
Iron Deposition ◽  
Direct Link ◽  
Transmission Electron ◽  
And Oxidative Stress

Background: Recent evidence suggests that the accumulation of iron, specifically ferrous Fe2+, may play a role in the development and progression of neurodegeneration in Alzheimer’s disease (AD) through the production of oxidative stress. Objective: To localize and characterize iron deposition and oxidation state in AD, we analyzed human hippocampal autopsy samples from four subjects with advanced AD that have been previously characterized with correlative MRI-histology. Methods: We perform scanning electron microscopy (SEM), energy dispersive spectroscopy (EDS), and electron energy loss spectroscopy (EELS) in the higher resolution transmission electron microscope on the surface and cross-sections of specific iron-rich regions of interest. Results: Specific previously analyzed regions were visualized using SEM and confirmed to be iron-rich deposits using EDS. Subsequent analysis using focused ion beam cross-sectioning and SEM characterized the iron deposition throughout the 3-D volumes, confirming the presence of iron throughout the deposits, and in two out of four specimens demonstrating colocalization with zinc. Analysis of traditional histology slides showed the analyzed deposits overlapped both with amyloid and tau deposition. Following higher resolution analysis of a single iron deposit using scanning transmission electron microscope (STEM), we demonstrated the potential of monochromated STEM-EELS to discern the relative oxidation state of iron within a deposit. Conclusion: These findings suggest that iron is present in the AD hippocampus and can be visualized and characterized using combined MRI and EM techniques. An altered relative oxidation state may suggest a direct link between iron and oxidative stress in AD. These methods thus could potentially measure an altered relative oxidation state that could suggest a direct link between iron and oxidative stress in AD. Furthermore, we have demonstrated the ability to analyze metal deposition alongside commonly used histological markers of AD pathology, paving the way for future insights into the molecular interactions between Aβ, tau, iron, and other putative metals, such as zinc.

The protective effects of carvacrol and thymol against paracetamol–induced toxicity on human hepatocellular carcinoma cell lines (HepG2)

2016 ◽  
Vol 35 (12) ◽  
pp. 1252-1263 ◽  
Author(s):  
SS Palabiyik ◽  
E Karakus ◽  
Z Halici ◽  
E Cadirci ◽  
Y Bayir ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Inflammatory Cytokines ◽  
Hepg2 Cells ◽  
Folk Medicine ◽  
Hepatoprotective Activity ◽  
High Dose ◽  
Protective Effects ◽  
And Oxidative Stress ◽  
Pro Inflammatory Cytokines

Acetaminophen (APAP) overdose could induce liver damage and lead to acute liver failure. The treatment of APAP overdoses could be improved by new therapeutic strategies. Thymus spp., which has many beneficial effects and has been used in folk medicine, is one such potential strategy. In the present study, the hepatoprotective activity of the main constituents of Thymus spp., carvacrol and thymol, were evaluated in light of APAP-induced hepatotoxicity. We hoped to understand the hepatoprotective mechanism of these agents on the antioxidant system and pro-inflammatory cytokines in vitro. Dose-dependent effects of thymol and carvacrol (25, 50, and 100 µM) were tested on cultured HepG2 cells. N-Acetylcysteine (NAC) was tested as positive control. We showed that APAP inhibited HepG2 cell growth by inducing inflammation and oxidative stress. Incubating APAP-exposed HepG2 cells with carvacrol and thymol for 24 h ameliorated this inflammation and oxidative stress. We also evaluated alanine transaminase and lactate dehydrogenase levels of HepG2 cells. We found that thymol and carvacrol protected against APAP-induced toxicity in HepG2 cells by increasing antioxidant activity and reducing pro-inflammatory cytokines, such as tumor necrosis factor α and interleukin 1β. Taking together high-dose thymol and carvacrol treatment has an effect close to NAC treatment in APAP toxicity, but thymol has better treatment effect than carvacrol.

Sign in / Sign up

Export Citation Format

Share Document