Effects of Pediatric Toothpastes Based on 500 to 1450 ppm Sodium Fluoride and Amine Fluoride with Different Detergents on Oxidative Stress and Cell Viability

Objective: Ischemia-reperfusion (I/R) injury is a pathological feature of ischemic stroke. This study investigated the regulatory role of miR-485-5p in I/R injury. Methods: SH-SY5Y cells were induced with oxygen and glucose deprivation/reoxygenation (OGD/R) to mimic I/R injury in vitro. Cells were transfected with designated constructs (miR-485- 5p mimics, miR-485-5p inhibitor, lentiviral vectors overexpressing Rac1 or their corresponding controls). Cell viability was evaluated using the MTT assay. The concentrations of lactate dehydrogenase, malondialdehyde, and reactive oxygen species were detected to indicate the degree of oxidative stress. Flow cytometry and caspase-3 activity assay were used for apoptosis assessment. Dual-luciferase reporter assay was performed to confirm that Rac family small GTPase 1 (Rac1) was a downstream gene of miR-485-5p. Results: OGD/R resulted in decreased cell viability, elevated oxidative stress, increased apoptosis, and downregulated miR-485-5p expression in SH-SY5Y cells. MiR-485-5p upregulation alleviated I/R injury, evidenced by improved cell viability, decreased oxidative markers, and reduced apoptotic rate. OGD/R increased the levels of Rac1 and neurogenic locus notch homolog protein 2 (Notch2) signaling-related proteins in cells with normal miR-485-5p expression, whereas miR- 485-5p overexpression successfully suppressed OGD/R-induced upregulation of these proteins. Furthermore, the delivery of vectors overexpressing Rac1 in miR-485-5p mimics-transfected cells reversed the protective effect of miR-485-5p in cells with OGD/R-induced injury. Conclusion: This study showed that miR-485-5p protected cells following I/R injury via targeting Rac1/Notch2 signaling suggest that targeted upregulation of miR-485-5p might be a promising therapeutic option for the protection against I/R injury.

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

Current Nutraceuticals ◽

10.2174/2665978601999200807160528 ◽

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.

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Effects of sodium fluoride and Ocimum sanctum extract on the lifespan and climbing ability of Drosophila melanogaster

The Journal of Basic and Applied Zoology ◽

10.1186/s41936-021-00229-8 ◽

2021 ◽

Vol 82 (1) ◽

Author(s):

Sidra Perveen ◽

Shalu Kumari ◽

Himali Raj ◽

Shahla Yasmin

Keyword(s):

Oxidative Stress ◽

Lipid Peroxidation ◽

Drosophila Melanogaster ◽

Sodium Fluoride ◽

Ocimum Sanctum ◽

Activity Assay ◽

Lipid Peroxidation Assay ◽

Climbing Ability ◽

The Impact ◽

Sublethal Concentrations

Abstract Background Fluoride may induce oxidative stress and apoptosis. It may also lead to neurobehavioural defects including neuromuscular damage. The present study aimed to explore the effects of sub lethal concentrations of sodium fluoride (NaF) on the lifespan and climbing ability of Drosophila melanogaster. In total, 0.6 mg/L and 0.8 mg/L of NaF were selected as sublethal concentrations of NaF for the study. Lifespan was measured and climbing activity assay was performed. Results The study showed significant decrease in lifespan of flies treated with fluoride. With increasing age, significant reduction in climbing activity was observed in flies treated with sodium fluoride as compared to normal (control) flies. Flies treated with tulsi (Ocimum sanctum) and NaF showed increase in lifespan and climbing activity as compared to those treated with NaF only. Lipid peroxidation assay showed significant increase in malondialdehyde (MDA) values in the flies treated with NaF as compared to control. The MDA values decreased significantly in flies treated with tulsi mixed with NaF. Conclusions The results indicate that exposure to sub lethal concentration of NaF may cause oxidative stress and affect the lifespan and climbing activity of D. melanogaster. Tulsi extract may help in reducing the impact of oxidative stress and toxicity caused by NaF.

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Cytotoxicity induced by new spiral mesoporous silica nanorods via specific surface area and ROS accumulation in HeLa cells

Materials Advances ◽

10.1039/d0ma00199f ◽

2020 ◽

Vol 1 (9) ◽

pp. 3556-3564

Author(s):

Lan She ◽

Miao Sun ◽

Xinfang Li ◽

Anfeng Kang ◽

Feng Yang ◽

...

Keyword(s):

Oxidative Stress ◽

Mesoporous Silica ◽

Cell Viability ◽

Specific Surface ◽

Surface Area ◽

Specific Surface Area ◽

Hela Cells ◽

Ros Accumulation ◽

Silica Nanorods

Results indicated that the effect of MSNRs on cell viability and cellular oxidative stress was related to specific surface area.

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In Vivo Protective Effects of Gallic Acid Isolated from Peltiphyllum Peltatum Against Sodium Fluoride-Induced Oxidative Stress in Rat Erythrocytes

Archives of Industrial Hygiene and Toxicology ◽

10.2478/10004-1254-64-2013-2353 ◽

2013 ◽

Vol 64 (4) ◽

pp. 553-559 ◽

Cited By ~ 12

Author(s):

Seyed Fazel Nabavi ◽

Solomon Habtemariam ◽

Antoni Sureda ◽

Akbar Hajizadeh Moghaddam ◽

Maria Daglia ◽

...

Keyword(s):

Oxidative Stress ◽

Lipid Peroxidation ◽

Superoxide Dismutase ◽

Vitamin C ◽

Gallic Acid ◽

Sodium Fluoride ◽

Enzyme Activities ◽

Control Group ◽

Rat Erythrocytes ◽

Pre Treatment

Abstract Gallic acid has been identified as an antioxidant component of the edible and medicinal plant Peltiphyllum peltatum. The present study examined its potential protective role against sodium fluoride (NaF)-induced oxidative stress in rat erythrocytes. Oxidative stress was induced by NaF administration through drinking water (1030.675 mg m-3 for one week). Gallic acid at 10 mg kg-1 and 20 mg kg-1 and vitamin C for positive controls (10 mg kg-1) were administered daily intraperitoneally for one week prior to NaF administration. Thiobarbituric acid reactive substances, antioxidant enzyme activities (superoxide dismutase and catalase), and the level of reduced glutathione were evaluated in rat erythrocytes. Lipid peroxidation in NaF-exposed rats significantly increased (by 88.8 %) when compared to the control group (p<0.05). Pre-treatment with gallic acid suppressed lipid peroxidation in erythrocytes in a dose-dependent manner. Catalase and superoxide dismutase enzyme activities and glutathione levels were reduced by NaF intoxication by 54.4 %, 63.69 %, and 42 % (p<0.001; vs. untreated control group), respectively. Pre-treatment with gallic acid or vitamin C significantly attenuated the deleterious effects. Gallic acid isolated from Peltiphyllum peltatum and vitamin C mitigated the NaF-induced oxidative stress in rat erythrocytes.

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Beneficial effect of 1,25 dihydroxyvitamin D3 on cytokine-treated human pancreatic islets

Journal of Endocrinology ◽

10.1677/joe.0.1690161 ◽

2001 ◽

Vol 169 (1) ◽

pp. 161-168 ◽

Cited By ~ 45

Author(s):

R Riachy ◽

B Vandewalle ◽

S Belaich ◽

J Kerr-Conte ◽

V Gmyr ◽

...

Keyword(s):

Oxidative Stress ◽

Vitamin D ◽

Cell Viability ◽

Pancreatic Islets ◽

Mhc Class I ◽

Class I ◽

Insulin Content ◽

Hsp70 Expression ◽

Human Pancreatic Islets ◽

Mnsod Activity

We examined whether 1,25 dihydroxyvitamin D(3) (1,25 D(3)), the active form of vitamin D involved in the regulation of the immune system, may also protect human pancreatic islet cells from destruction induced by cytokines. In this study, we specifically investigated the effect of 1,25 D(3) on oxidative stress and major histocompatibility complex (MHC) induction, both implicated in cytokine-induced islet cell dysfunction and destruction. We also investigated the effects of 1,25 D(3) on interleukin (IL)-6, a pleiotropic cytokine implicated in the pathogenesis of immunoinflammatory disorders. Human pancreatic islets, isolated from heart-beating donors, were treated with a combination of three cytokines, IL-1beta+tumor necrosis factor alpha+interferon gamma, in the presence or absence of vitamin D, and compared with with untreated control cells. Metabolic activity was assessed by cell viability and insulin content. Oxidative stress was estimated by heat shock protein 70 (hsp70) expression, cell manganese superoxide dismutase (MnSOD) activity and nitrite release, a reflexion of nitric oxide (NO) synthesis. Variation of immunogenicity of islet preparations was determined by analysis of the MHC class I and class II transcripts. Inflammatory status was evaluated by IL-6 production. After 48 h of contact with cytokines, insulin content was significantly decreased by 40% but cell viability was not altered. MHC expression significantly increased six- to sevenfold as well as NO and IL-6 release (two- to threefold enhancement). MnSOD activity was not significantly induced and hsp70 expression was not affected by the combination of cytokines. The addition of 1,25 D(3) significantly reduced nitrite release, IL-6 production and MHC class I expression which then became not significantly different from controls. These results suggest that the effect of 1,25 D(3) in human pancreatic islets cells may be a reduction of the vulnerability of cells to cytotoxic T lymphocytes and a reduction of cytotoxic challenge. Hence, 1,25 D(3) might play a role in the prevention of type 1 diabetes and islet allograft rejection.

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Toxicity of Cerium Oxide Nanoparticles in Human Lung Cancer Cells

International Journal of Toxicology ◽

10.1080/10915810600959543 ◽

2006 ◽

Vol 25 (6) ◽

pp. 451-457 ◽

Cited By ~ 319

Author(s):

Weisheng Lin ◽

Yue-wern Huang ◽

Xiao-Dong Zhou ◽

Yinfa Ma

Keyword(s):

Oxidative Stress ◽

Lung Cancer ◽

Lactate Dehydrogenase ◽

Cell Viability ◽

Cancer Cells ◽

Cerium Oxide ◽

Human Lung ◽

Lung Cancer Cells ◽

Human Lung Cancer ◽

Human Lung Cancer Cells

With the fast development of nanotechnology, the nanomaterials start to cause people’s attention for potential toxic effect. In this paper, the cytotoxicity and oxidative stress caused by 20-nm cerium oxide (CeO2) nanoparticles in cultured human lung cancer cells was investigated. The sulforhodamine B method was employed to assess cell viability after exposure to 3.5, 10.5, and 23.3 μg/ml of CeO2 nanoparticles for 24, 48, and 72 h. Cell viability decreased significantly as a function of nanoparticle dose and exposure time. Indicators of oxidative stress and cytotoxicity, including total reactive oxygen species, glutathione, malondialdehyde, α-tocopherol, and lactate dehydrogenase, were quantitatively assessed. It is concluded from the results that free radicals generated by exposure to 3.5 to 23.3 μg/ml CeO2 nanoparticles produce significant oxidative stress in the cells, as reflected by reduced glutathione and α-tocopherol levels; the toxic effects of CeO2 nanoparticles are dose dependent and time dependent; elevated oxidative stress increases the production of malondialdehyde and lactate dehydrogenase, which are indicators of lipid peroxidation and cell membrane damage, respectively.

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Neuroprotective effects of silymarin on sodium fluoride-induced oxidative stress

Journal of Fluorine Chemistry ◽

10.1016/j.jfluchem.2012.06.029 ◽

2012 ◽

Vol 142 ◽

pp. 79-82 ◽

Cited By ~ 15

Author(s):

Seyed Mohammad Nabavi ◽

Antoni sureda ◽

Seyed Fazel Nabavi ◽

Ali Mohammad Latifi ◽

Akbar Hajizadeh Moghaddam ◽

...

Keyword(s):

Oxidative Stress ◽

Sodium Fluoride ◽

Neuroprotective Effects

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Matrine Protects PC12 Cells Against Aβ25–35-Induced Cytotoxicity, Oxidative Stress, Inflammation, Neuronal Apoptosis and Cell Senescence

Journal of Biomaterials and Tissue Engineering ◽

10.1166/jbt.2021.2603 ◽

2021 ◽

Vol 11 (9) ◽

pp. 1691-1697

Author(s):

Huanli Zhang ◽

Zhen Zhang

Keyword(s):

Oxidative Stress ◽

Cell Viability ◽

Pc12 Cells ◽

Neuronal Apoptosis ◽

Inflammatory Responses ◽

Neuronal Damage ◽

Cell Senescence ◽

Tunel Staining ◽

Elisa Assay ◽

Amyloid A

Background and Objectives: Beta-amyloid (Aβ) has pivotal functions in the pathogenesis of Alzheimer’s Disease (AD). The main purpose of this study is to explore the protective role and possible mechanisms of matrine against Aβ25–35-induced neurotoxicity in PC12 cells. Materials and Methods: A vitro model that involved Aβ25–35-induced neuronal damage in PC12 cells was adopted in the present study. Cell viability and apoptosis of PC12 cells were determined by CCK-8 assay and TUNEL staining, respectively. Intracellular ROS levels were determined by DCFH-DA probe and levels of TNFα, IL-6 and IL-1β were assessed by ELISA assay. In addition, telomerase reverse transcriptase (TERT) levels were determined by ELISA assay and telomere lengths were examined by real-time quantitative PCR analysis to assess telomerase activities. Furthermore, vital proteins related to cell apoptosis and hallmarks of senescence were detected by western blot analysis. Results: Matrine (10, 20, 50 μg/ml) dose-dependently protected cell viability against Aβ25–35 cytotoxicity in PC12 cells. Meanwhile, matrine at 10, 20, 50 μg/ml markedly reduced ROS production and downregulated the levels of TNFα, IL-6 and IL-1β in Aβ25–35-injuried PC12 cells. The results also proved that matrine may restore telomerase activities and telomere lengths in Aβ25–35-injuried PC12 cells by inhibiting inflammatory responses and oxidative stress. Neuronal apoptosis induced by Aβ25–35 were reversed upon cotreatment with matrine. Moreover, matrine markedly mitigated Aβ25–35 induced cell senescence in a concentration-dependentmanner. Conclusion: Our findings demonstrated that matrine protected PC12 cells against Aβ25–35-induced cytotoxicity, oxidative stress, inflammation, neuronal apoptosis and cell senescence.

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Silibinin-Albumin Nanoparticles: Characterization and Biological Evaluation Against Oxidative Stress-Stimulated Neurotoxicity Associated with Alzheimer’s Disease

Journal of Biomedical Nanotechnology ◽

10.1166/jbn.2021.3038 ◽

2021 ◽

Vol 17 (6) ◽

pp. 1123-1130

Author(s):

Qichen Pan ◽

Yunchao Ban ◽

Lijun Xu

Keyword(s):

Oxidative Stress ◽

Alzheimer’S Disease ◽

Alzheimer's Disease ◽

Antioxidant Activity ◽

Cell Viability ◽

Antioxidant Activities ◽

Drug Loading ◽

Biological Evaluation ◽

Neural Cells ◽

Nanoparticles Characterization

Alzheimer’s disease (AD) is strongly associated with oxidative stress which can damage neural cells. Silibinin has shown potential antioxidative effects. However, due to its low solubility in water, silibinin provides low biological activity and bioavailability. Therefore, to increase its pharmacological effects, silibilin was encapsulated into human serum albumin (HSA) nanoparticles and well-characterized by DLS and TEM techniques. The antioxidant activity of silibinin-HSA nanoparticles was evaluated on LPS-induced oxidative stress in neuron-like cells (SH-SY5Y) through MTT, antioxidant activity and apoptotic assay. It was shown that the mean diameter of HSA and silibinin-HSA nanoparticles were 88 and 105 nm, respectively with a drug loading of 24.08%, drug encapsulation rate of 94.72%, and the yield of silibinin-HSA nanoparticles of around 83.41% and the HSA nano-formulation released silibinin for 15 h. The results displayed that cell viability was reduced by LPS (10 μg/mL), who’s also determined to stimulate oxidative stress and apoptosis. However, co-incubation of cells with silibinin (50 μg/mL) or silibinin-HSA nanoparticles led to the recovery of cell viability, activation of SOD and CAT, increase of GSH content, and reduction of ROS level, Caspase-3 activity and fragmentation of DNA. It was also indicated that the neuroprotective and antioxidant activities of silibinin-HAS nanoparticles was greater than free silibinin, indicating that using albumin can be a potential formulation approach for improving the antioxidant efficacy of silibinin.

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