scholarly journals Graphene Oxide–Silver Nanoparticle Nanocomposites Induce Oxidative Stress and Aberrant Methylation in Caprine Fetal Fibroblast Cells

Cells ◽  
2021 ◽  
Vol 10 (3) ◽  
pp. 682
Author(s):  
Yu-Guo Yuan ◽  
He-Qing Cai ◽  
Jia-Lin Wang ◽  
Ayman Mesalam ◽  
Abu Md Talimur Reza ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Graphene Oxide ◽  
Silver Nanoparticle ◽  
Cell Counting ◽  
Aberrant Methylation ◽  
Fibroblast Cells ◽  
Dependent Manner ◽  
Dna Hypomethylation ◽  
Fetal Fibroblast ◽  
Apoptotic Genes

Graphene oxide–silver nanoparticle (GO-AgNPs) nanocomposites have drawn much attention for their potential in biomedical uses. However, the potential toxicity of GO-AgNPs in animals and humans remains unknown, particularly in the developing fetus. Here, we reported the GO-AgNP-mediated cytotoxicity and epigenetic alteration status in caprine fetal fibroblast cells (CFFCs). In brief, the proliferation and apoptosis rate of GO-AgNP-treated CFFCs (4 and 8 µg/mL of GO-AgNPs) were measured using the cell-counting kit (CCK-8) assay and the annexin V/propidium iodide (PI) assay, respectively. In addition, the oxidative stress induced by GO-AgNPs and detailed mechanisms were studied by evaluating the generation of reactive oxygen species (ROS), superoxide dismutase (SOD), lactate dehydrogenase (LDH), malondialdehyde (MDA), and caspase-3 and abnormal methylation. The expression of pro- and anti-apoptotic genes and DNA methyltransferases was measured using reverse transcription followed by RT-qPCR. Our data indicated that GO-AgNPs cause cytotoxicity in a dose-dependent manner. GO-AgNPs induced significant cytotoxicity by the loss of cell viability, production of ROS, increasing leakage of LDH and level of MDA, increasing expression of pro-apoptotic genes, and decreasing expression of anti-apoptotic genes. GO-AgNPs incited DNA hypomethylation and the decreased expression of DNMT3A. Taken together, this study showed that GO-AgNPs increase the generation of ROS and cause apoptosis and DNA hypomethylation in CFFCs. Therefore, the potential applications of GO-AgNPs in biomedicine should be re-evaluated.

scholarly journals Graphene oxide-silver nanocomposites induce oxidative stress and apoptosis in caprine fetal fibroblast cells

2020 ◽  
Author(s):  
Yu-Guo Yuan ◽  
Myeong-Don Joo ◽  
Jia-Lin Wang ◽  
Ayman Mesalam ◽  
Abu Musa Md Talimur R ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Silver Nanoparticles ◽  
Graphene Oxide ◽  
Fibroblast Cell ◽  
Dependent Manner ◽  
Potential Toxicity ◽  
Fetal Fibroblast ◽  
Reduced Graphene ◽  
Apoptotic Genes ◽  
Dose Dependent

Abstract Background: Graphene oxide (GO) has drawn much attention as excellent platform to which silver nanoparticles (AgNPs) can be anchored for the production of biomedical nanocomposites. Yet, the potential toxicity of reduced graphene oxide- silver nanoparticles (GO-AgNPs) nanocomposites to animal and human is complex to evaluate and remains largely unknown.Results: Our data indicated that GO-AgNPs caused cytotoxicity in dose-dependent manner. GO-AgNPs induced significant cytotoxicity by the loss of cell viability, over-production of reactive oxygen species (ROS), increased leakage of lactate dehydrogenase (LDH) and level of malondialdehyde (MDA), increased expression of pro-apoptotic genes and decreased expression of anti-apoptotic genes.Conclusions: This study demonstrated that GO-AgNPs potentially induced oxidative stress, which resulted in toxicity and cell apoptosis in caprine fetal fibroblast cell due to an increased generation of ROS. For antibacterial applications of GO-AgNPs nanocomposite in animal, the toxical effect must be further evaluated.

scholarly journals Graphene oxide-silver nanoparticle nanocomposites induces apoptosis in caprine fetal fibroblast cells via induction of oxidative stress

2020 ◽  
Author(s):  
Yu-Guo Yuan ◽  
Myeong-Don Joo ◽  
Jia-Lin Wang ◽  
Ayman Mesalam ◽  
Abu Musa Md Talimur R ◽  
...  
Keyword(s):  
Graphene Oxide ◽  
Fibroblast Cell ◽  
Dependent Manner ◽  
Oxygen Species ◽  
Potential Toxicity ◽  
Fetal Fibroblast ◽  
Cycle Arrest ◽  
Apoptotic Genes ◽  
Oxidative Damage To Dna ◽  
Dose Dependent

Abstract Background: Graphene oxide (GO) has drawn much attention as excellent platform to which silver nanoparticles (AgNPs) can be anchored for the production of biomedical nanocomposites. Yet, the potential toxicity of GO-AgNPs nanocomposites to animal and human is complex to evaluate and remains largely unknown. Results: Our data indicated that GO-AgNPs caused cytotoxicity in dose-dependent manner. GO-AgNPs induced significant cytotoxicity by the loss of cell viability, production of reactive oxygen species (ROS), cell cycle arrest, increasing leakage of lactate dehydrogenase (LDH) and level of Malondialdehyde (MDA), increasing expression of pro-apoptotic genes and decreasing expression of anti-apoptotic genes. Conclusions: Taken together, our study demonstrated that GO-AgNPs potentially induce oxidative damage to DNA, which result in toxicity and cell apoptosis in caprine fetal fibroblast cell due to an increased generation of ROS. It strongly suggests that applications of GO-AgNPs nanocomposite in animal must be further evaluated.

scholarly journals Hydrogen Sulfide Protects against Chemical Hypoxia-Induced Injury via Attenuation of ROS-Mediated Ca2+Overload and Mitochondrial Dysfunction in Human Bronchial Epithelial Cells

2018 ◽  
Vol 2018 ◽  
pp. 1-9 ◽  
Author(s):  
Cai-Xia Liu ◽  
Yu-Rong Tan ◽  
Yang Xiang ◽  
Chi Liu ◽  
Xiao-Ai Liu ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Hydrogen Sulfide ◽  
Cell Injury ◽  
Fluorescence Probe ◽  
Environmental Pollutants ◽  
Cell Counting ◽  
Dependent Manner ◽  
Mitochondria Membrane Potential ◽  
Chemical Hypoxia ◽  
The Impact

Oxidative stress induced by hypoxia/ischemia resulted in the excessive reactive oxygen species (ROS) and the relative inadequate antioxidants. As the initial barrier to environmental pollutants and allergic stimuli, airway epithelial cell is vulnerable to oxidative stress. In recent years, the antioxidant effect of hydrogen sulfide (H2S) has attracted much attention. Therefore, in this study, we explored the impact of H2S on CoCl2-induced cell injury in 16HBE14o- cells. The effect of CoCl2on the cell viability was detected by Cell Counting Kit (CCK-8) and the level of ROS in 16HBE14o- cells in response to varying doses (100–1000μmol/L) of CoCl2(a common chemical mimic of hypoxia) was measured by using fluorescent probe DCFH-DA. It was shown that, in 16HBE14o- cells, CoCl2acutely increased the ROS content in a dose-dependent manner, and the increased ROS was inhibited by the NaHS (as a donor of H2S). Moreover, the calcium ion fluorescence probe Fura-2/AM and fluorescence dye Rh123 were used to investigate the intracellular calcium concentration ([Ca2+]i) and mitochondria membrane potential (MMP) in 16HBE14o- cells, respectively. In addition, we examined apoptosis of 16HBE14o- cells with Hoechst 33342. The results showed that the CoCl2effectively elevated the Ca2+influx, declined the MMP, and aggravated apoptosis, which were abrogated by NaHS. These results demonstrate that H2S could attenuate CoCl2-induced hypoxia injury via reducing ROS to perform an agonistic role for the Ca2+influx and MMP dissipation.

scholarly journals Cobalt Chloride Alters Mitochondrial Function in a Dose Dependent Manner

2021 ◽  
Vol 37 (3) ◽  
Author(s):  
Pham Thi Bich ◽  
Vu Thi Thu
Keyword(s):  
Oxidative Stress ◽  
Mitochondrial Function ◽  
Mitochondrial Membrane ◽  
Cobalt Chloride ◽  
Dose Dependence ◽  
Cell Counting ◽  
Dependent Manner ◽  
Mitochondrial Oxidative Stress ◽  
H9c2 Cardiomyocytes ◽  
Dose Dependent

Aim: This study was carried to evaluates of Cobalt chloride (CoCl2) on cardiac mitochondrial function. Methods: H9C2 cardiomyocytes were cultured in medium containing different concentrations of CoCl2. Cell viability, cardiolipin content, mitochondrial function, and mitochondrial oxidative stress were assessed by using Cell Counting Kit-8 and suitable fluorescence kits. Results: The obtained data showed that CoCl2 (200÷400 µM) induced cell death and decreased mitochondrial function of H9C2 cardiomyocytes in dose dependence. Especially, CoCl2 at dose of 300 µM significantly altered values of mitochondrial membrane potential, H2O2 and O2- to 63.79±2.15%, 145.81±5.83% and 143.10±3.07% (of 100% control), respectively. Conclusion: CoCl2 strongly induced cardiomyocyte death via altering mitochondrial function in a dose-dependent manner.

Cytoprotective effects of the aqueous extract of the Ziziphus jujuba fruit on TBHP-induced damage on human fibroblast cells

2019 ◽  
Vol 31 (3) ◽  
Author(s):  
Mina Arab ◽  
Mohsen Khorashadizadeh ◽  
Zahra Abotorabi ◽  
Asghar Zarban
Keyword(s):  
Oxidative Stress ◽  
Antioxidant Activity ◽  
Cell Viability ◽  
Aqueous Extract ◽  
Human Fibroblast ◽  
Fibroblast Cells ◽  
Dependent Manner ◽  
Antioxidant Power ◽  
Human Fibroblast Cells ◽  
Ziziphus Jujuba

AbstractBackgroundOxidative stress plays a major role in the development of various human diseases. However, many antioxidant compounds can neutralize the excess of free radicals, protect the cells against their toxic effects and help prevent or treat a disease. This study investigated the cytoprotective effects of the aqueous extract of the Ziziphus jujuba fruit on the tert-butyl hydroperoxide (TBHP)-induced damage on human fibroblast cells.MethodsHuman fibroblast cells were pretreated with different concentrations (1, 2, 4, 8 mg/mL) of Z. jujuba for 24 h and exposed to 75 μM TBHP for another 24 h. Cell viability was determined by the MTT assay. The antioxidant activity was determined using the 2, 2-diphenyl-1-picrylhydrazyl (DPPH) and ferric reducing antioxidant power (FRAP) methods, and the intracellular antioxidant activity was evaluated with the Cellular antioxidant activity assay.ResultsOur data showed that treatment with TBHP reduced cell viability of human fibroblast cells, while pretreatment with Z. jujuba increased cell viability in a dose-dependent manner. This indicated the cytoprotective effects of Z. jujuba. Pretreatment with Z. jujuba increased the antioxidant capacity and scavenged the TBHP-produced peroxyl radicals in the human fibroblast cell medium. Moreover, Z. jujuba increased the intracellular antioxidant activity of human fibroblast cells.ConclusionsThese results demonstrated that the aqueous extract of the Z. jujuba fruit can prevent TBHP-induced cellular toxicity by enhancing the antioxidant activity in cells and their medium. So, Z. jujuba has a therapeutic potential to attenuate oxidative stress-induced diseases.

Synergism of Temozolomide, Metformin and Epigallocatechin Gallate Promotes Oxidative Stress-induced Apoptosis in Glioma Cells

2021 ◽  
Vol 16 ◽  
Author(s):  
Shreyas S. Kuduvalli ◽  
Daisy Precilla S. ◽  
A. Vinodhini ◽  
T. S. Anitha
Keyword(s):  
Oxidative Stress ◽  
Drug Combination ◽  
Epigallocatechin Gallate ◽  
Glioma Cells ◽  
C6 Glioma ◽  
C6 Glioma Cells ◽  
Dependent Manner ◽  
Caspase 9 ◽  
Apoptotic Genes ◽  
Induced Apoptosis

Aim: To study the synergistic anti-glioma efficacies of Temozolomide, Metformin and Epigallocatechin Gallate in U87MG and C6 glioma cells. Background: Glioblastoma (GBM) is the most malignant and invasive tumor of the central nervous system. The current standard treatment comprises surgical resection, followed by adjuvant radiotherapy and chemotherapy employing temozolomide (TMZ). Yet the survival rates for GBM patients is very low. Hence there is a need for new treatment regimes Objective: This study was aimed to unravel the synergistic anti-tumor potential of a biguanide drug, Metformin (MET) and a polyphenol, Epigallocatechin gallate (EGCG) to enhance the anti-GBM efficacy of the standard drug. Methods: Anti-proliferative effect of TMZ, MET and EGCG, individually and in combination was elucidated in U87MG (human) and C6 (rat) glioma cells using MTT assay and combination index was used to determine synergism. Cytotoxicity of the drugs was performed in HEK293T noncancerous cells. Apoptotic morphological changes in the cells were observed by AO/EtBr staining. Further, the effect of drugs on antioxidant and apoptotic genes (SOD, CAT, Nrf-2, Caspase-9 and Bcl-2) were evaluated using qRT-PCR and the protein levels of Nrf-2 and Caspase-9 was evaluated using ELISA. Results: The triple-drug combination (TMZ+ MET+ EGCG) synergistically inhibited the proliferation of U87MG and C6 glioma cells in a dose-dependent manner and promoted the apoptosis of glioma cells. The triple-drug combination significantly up-regulated the expression of antioxidant and apoptotic genes and induced oxidative stress suggesting a shift in equilibrium towards apoptosis. Conclusion: MET and EGCG in combination with TMZ synergistically promoted oxidative stress induced apoptosis in glioma cells. Hence, the combination of TMZ, MET and EGCG may be therapeutically exploited for improving the clinical outcomes of patients with GBM.

Non-canonical Functions of Telomerase Reverse Transcriptase: Emerging Roles and Biological Relevance

2020 ◽  
Vol 20 (6) ◽  
pp. 498-507 ◽  
Author(s):  
Connor A.H. Thompson ◽  
Judy M.Y. Wong
Keyword(s):  
Oxidative Stress ◽  
Dna Damage ◽  
Reverse Transcriptase ◽  
Cancer Cells ◽  
Telomere Length ◽  
Telomere Maintenance ◽  
Telomerase Reverse Transcriptase ◽  
Alternative Mechanism ◽  
Dependent Manner ◽  
Mitochondrial Integrity

Increasing evidence from research on telomerase suggests that in addition to its catalytic telomere repeat synthesis activity, telomerase may have other biologically important functions. The canonical roles of telomerase are at the telomere ends where they elongate telomeres and maintain genomic stability and cellular lifespan. The catalytic protein component Telomerase Reverse Transcriptase (TERT) is preferentially expressed at high levels in cancer cells despite the existence of an alternative mechanism for telomere maintenance (alternative lengthening of telomeres or ALT). TERT is also expressed at higher levels than necessary for maintaining functional telomere length, suggesting other possible adaptive functions. Emerging non-canonical roles of TERT include regulation of non-telomeric DNA damage responses, promotion of cell growth and proliferation, acceleration of cell cycle kinetics, and control of mitochondrial integrity following oxidative stress. Non-canonical activities of TERT primarily show cellular protective effects, and nuclear TERT has been shown to protect against cell death following double-stranded DNA damage, independent of its role in telomere length maintenance. TERT has been suggested to act as a chromatin modulator and participate in the transcriptional regulation of gene expression. TERT has also been reported to regulate transcript levels through an RNA-dependent RNA Polymerase (RdRP) activity and produce siRNAs in a Dicer-dependent manner. At the mitochondria, TERT is suggested to protect against oxidative stress-induced mtDNA damage and promote mitochondrial integrity. These extra-telomeric functions of TERT may be advantageous in the context of increased proliferation and metabolic stress often found in rapidly-dividing cancer cells. Understanding the spectrum of non-canonical functions of telomerase may have important implications for the rational design of anti-cancer chemotherapeutic drugs.

Combination of Histone Deacetylase Inhibitor with Cu(II) 5,5- diethylbarbiturate Complex Induces Apoptosis in Breast Cancer Stem Cells: A Promising Novel Approach

2020 ◽  
Vol 21 ◽  
Author(s):  
Merve Erkisa ◽  
Nazlihan Aztopal ◽  
Elif Erturk ◽  
Engin Ulukaya ◽  
Veysel T. Yilmaz ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Oxidative Stress ◽  
Stem Cells ◽  
Cancer Stem Cells ◽  
Histone Deacetylases ◽  
Caspase 3 ◽  
Cancer Cell Line ◽  
Annexin V ◽  
Tumor Formation ◽  
Dependent Manner

Background: Cancer stem cells (CSC) are subpopulation within the tumor that acts a part in the initiation, progression, recurrence, resistance to drugs and metastasis of cancer. It is well known that epigenetic changes lead to tumor formation in cancer stem cells and show drug resistance. Epigenetic modulators and /or their combination with different agents have been used in cancer therapy. Objective: In our study we scope out the effects of combination of a histone deacetylases inhibitor, valproic acid (VPA), and Cu(II) complex [Cu(barb-κN)(barb-κ2N,O)(phen-κN,N’)]·H2O] on cytotoxicity/apoptosis in a stem-cell enriched population (MCF-7s) obtained from parental breast cancer cell line (MCF-7). Methods: Viability of the cells was measured by the ATP assay. Apoptosis was elucidated via the assessment of caspase-cleaved cytokeratin 18 (M30 ELISA) and a group of flow cytometry analysis (caspase 3/7 activity, phosphatidylserine translocation by annexin V-FITC assay, DNA damage and oxidative stress) and 2ˈ,7ˈ–dichlorofluorescein diacetate staining. Results: The VPA combined with Cu(II) complex showed anti proliferative activity on MCF-7s cells in a dose- and time-dependently. Treatment with combination of 2.5 mM VPA and 3.12 μM Cu(II) complex induces oxidative stress in a time-dependent manner, as well as apoptosis that is evidenced by the increase in caspase 3/7 activity, positive annexin-V-FITC, and increase in M30 levels. Conclusion: The results suggest that the combination therapy induces apoptosis following increased oxidative stress, thereby making it a possible promising therapeutic strategy that further analysis is required.

scholarly journals Silver nanoparticle-graphene oxide mixture as anti-bacterial against Staphylococcus aureus

2019 ◽  
Author(s):  
Wipsar Sunu Brams Dwandaru ◽  
Afrizal Lathiful Fadli ◽  
Dani Rahmawati Hakim ◽  
Absari Hanifah ◽  
Emi Kurnia Sari
Keyword(s):  
Staphylococcus Aureus ◽  
Graphene Oxide ◽  
Silver Nanoparticle ◽  
Oxide Mixture
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