scholarly journals Lauric Acid, a Dietary Saturated Medium-Chain Fatty Acid, Elicits Calcium-Dependent Eryptosis

Cells ◽  
2021 ◽  
Vol 10 (12) ◽  
pp. 3388
Author(s):  
Mohammad A. Alfhili ◽  
Ghadeer S. Aljuraiban
Keyword(s):  
Oxidative Stress ◽  
Lauric Acid ◽  
Dietary Habits ◽  
Saturated Fatty Acids ◽  
Annexin V ◽  
Lipid Peroxides ◽  
Dietary Interventions ◽  
Selective Toxicity ◽  
Neutrophil Lymphocyte Ratio ◽  
Calcium Dependent

Cardiovascular diseases (CVD) are a leading cause of mortality worldwide, and dietary habits represent a major risk factor for dyslipidemia; a hallmark of CVD. Saturated fatty acids contribute to CVD by aggravating dyslipidemia, and, in particular, lauric acid (LA) raises circulating cholesterol levels. The role of red blood cells (RBCs) in CVD is increasingly being appreciated, and eryptosis has recently been identified as a novel mechanism in CVD. However, the effect of LA on RBC physiology has not been thoroughly investigated. RBCs were isolated from heparin-anticoagulated whole blood (WB) and exposed to 50–250 μM of LA for 24 h at 37 °C. Hemoglobin was photometrically examined as an indicator of hemolysis, whereas eryptosis was assessed by Annexin V-FITC for phosphatidylserine (PS) exposure, Fluo4/AM for Ca2+, light scatter for cellular morphology, H2DCFDA for oxidative stress, and BODIPY 581/591 C11 for lipid peroxidation. WB was also examined for RBC, leukocyte, and platelet viability and indices. LA caused dose-responsive hemolysis, and Ca2+-dependent PS exposure, elevated erythrocyte sedimentation rate (ESR), cytosolic Ca2+ overload, cell shrinkage and granularity, oxidative stress, accumulation of lipid peroxides, and stimulation of casein kinase 1α (CK1α). In WB, LA disrupted leukocyte distribution with elevated neutrophil-lymphocyte ratio (NLR) due to selective toxicity to lymphocytes. In conclusion, this report provides the first evidence of the pro-eryptotic potential of LA and associated mechanisms, which informs dietary interventions aimed at CVD prevention and management.

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 Detection of Dysbiosis and Increased Intestinal Permeability in Brazilian Patients with Relapsing–Remitting Multiple Sclerosis

2021 ◽  
Vol 18 (9) ◽  
pp. 4621
Author(s):  
Felipe Papa Pellizoni ◽  
Aline Zazeri Leite ◽  
Nathália de Campos Rodrigues ◽  
Marcelo Jordão Ubaiz ◽  
Marina Ignácio Gonzaga ◽  
...  
Keyword(s):  
Multiple Sclerosis ◽  
Gut Microbiota ◽  
Intestinal Permeability ◽  
Dietary Habits ◽  
Dietary Interventions ◽  
Chi Square ◽  
16S Sequencing ◽  
Intestinal Dysbiosis ◽  
Relapsing Remitting ◽  
Relapsing Remitting Multiple Sclerosis

Dysbiosis, associated with barrier disruption and altered gut–brain communications, has been associated with multiple sclerosis (MS). In this study, we evaluated the gut microbiota in relapsing–remitting patients (RRMS) receiving disease-modifying therapies (DMTs) and correlated these data with diet, cytokines levels, and zonulin concentrations. Stool samples were used for 16S sequencing and real-time PCR. Serum was used for cytokine determination by flow cytometry, and zonulin quantification by ELISA. Pearson’s chi-square, Mann–Whitney, and Spearman’s correlation were used for statistical analyses. We detected differences in dietary habits, as well as in the gut microbiota in RRMS patients, with predominance of Akkermansia muciniphila and Bacteroides vulgatus and decreased Bifidobacterium. Interleukin-6 concentrations were decreased in treated patients, and we detected an increased intestinal permeability in RRMS patients when compared with controls. We conclude that diet plays an important role in the composition of the gut microbiota, and intestinal dysbiosis, detected in RRMS patients could be involved in increased intestinal permeability and affect the clinical response to DTMs. The future goal is to predict therapeutic responses based on individual microbiome analyses (personalized medicine) and propose dietary interventions and the use of probiotics or other microbiota modulators as adjuvant therapy to enhance the therapeutic efficacy of DMTs.

scholarly journals Alleviation of Memory Deficit by Bergenin via the Regulation of Reelin and Nrf-2/NF-κB Pathway in Transgenic Mouse Model

2021 ◽  
Vol 22 (12) ◽  
pp. 6603
Author(s):  
Bushra Shal ◽  
Adnan Khan ◽  
Ashraf Ullah Khan ◽  
Rahim Ullah ◽  
Gowhar Ali ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Mouse Model ◽  
Neuroprotective Effect ◽  
Annexin V ◽  
Memory Deficit ◽  
Y Maze ◽  
Spatial Memory Deficit ◽  
Aβ Aggregation ◽  
Ft Ir ◽  
Reelin Signaling

The present study aims to determine the neuroprotective effect of Bergenin against spatial memory deficit associated with neurodegeneration. Preliminarily, the protective effect of Bergenin was observed against H2O2-induced oxidative stress in HT-22 and PC-12 cells. Further studies were performed in 5xFAD Tg mouse model by administering Bergenin (1, 30 and 60 mg/kg; orally), whereas Bergenin (60 mg/kg) significantly attenuated the memory deficit observed in the Y-maze and Morris water maze (MWM) test. Fourier transform-infrared (FT-IR) spectroscopy displayed restoration of lipids, proteins and their derivatives compared to the 5xFAD Tg mice group. The differential scanning calorimeter (DSC) suggested an absence of amyloid beta (Aβ) aggregation in Bergenin-treated mice. The immunohistochemistry (IHC) analysis suggested the neuroprotective effect of Bergenin by increasing Reelin signaling (Reelin/Dab-1) and attenuated Aβ (1–42) aggregation in hippocampal regions of mouse brains. Furthermore, IHC and western blot results suggested antioxidant (Keap-1/Nrf-2/HO-1), anti-inflammatory (TLR-4/NF-kB) and anti-apoptotic (Bcl-2/Bax/Caspase-3) effect of Bergenin. Moreover, a decrease in Annexin V/PI-stained hippocampal cells suggested its effect against neurodegeneration. The histopathological changes were reversed significantly by Bergenin. In addition, a remarkable increase in antioxidant level with suppression of pro-inflammatory cytokines, oxidative stress and nitric oxide production were observed in specific regions of the mouse brains.

scholarly journals Brown Algae Phlorotannins: A Marine Alternative to Break the Oxidative Stress, Inflammation and Cancer Network

Foods ◽  
2021 ◽  
Vol 10 (7) ◽  
pp. 1478
Author(s):  
Marcelo D. Catarino ◽  
Sónia J. Amarante ◽  
Nuno Mateus ◽  
Artur M. S. Silva ◽  
Susana M. Cardoso
Keyword(s):  
Oxidative Stress ◽  
Physical Inactivity ◽  
Dietary Habits ◽  
Vegetable Intake ◽  
Fruit And Vegetable Intake ◽  
Bioactive Properties ◽  
Ability To Act ◽  
Pharmaceutical Industries ◽  
Biochemical Mechanisms ◽  
Cancer Network

According to the WHO, cancer was responsible for an estimated 9.6 million deaths in 2018, making it the second global leading cause of death. The main risk factors that lead to the development of this disease include poor behavioral and dietary habits, such as tobacco use, alcohol use and lack of fruit and vegetable intake, or physical inactivity. In turn, it is well known that polyphenols are deeply implicated with the lower rates of cancer in populations that consume high levels of plant derived foods. In this field, phlorotannins have been under the spotlight in recent years since they have shown exceptional bioactive properties, with great interest for application in food and pharmaceutical industries. Among their multiple bioactive properties, phlorotannins have revealed the capacity to interfere with several biochemical mechanisms that regulate oxidative stress, inflammation and tumorigenesis, which are central aspects in the pathogenesis of cancer. This versatility and ability to act either directly or indirectly at different stages and mechanisms of cancer growth make these compounds highly appealing for the development of new therapeutical strategies to address this world scourge. The present manuscript revises relevant studies focusing the effects of phlorotannins to counteract the oxidative stress–inflammation network, emphasizing their potential for application in cancer prevention and/or treatment.

scholarly journals Evaluation of Nutrient Intake and Food Consumption among Dutch Toddlers

Nutrients ◽  
2021 ◽  
Vol 13 (5) ◽  
pp. 1531
Author(s):  
Elly Steenbergen ◽  
Anne Krijger ◽  
Janneke Verkaik-Kloosterman ◽  
Liset E. M. Elstgeest ◽  
Sovianne ter Borg ◽  
...  
Keyword(s):  
Fatty Acids ◽  
Dietary Intake ◽  
Food Consumption ◽  
Dietary Habits ◽  
Saturated Fatty Acids ◽  
Dietary Guidelines ◽  
Food Groups ◽  
Milk Products ◽  
Health Council ◽  
Dutch Health

Improving dietary habits at a young age could prevent adverse health outcomes. The aim was to gain insight into the adequacy of the dietary intake of Dutch toddlers, which may provide valuable information for preventive measures. Data obtained from the Dutch National Food Consumption Survey 2012–2016 were used, which included 672 children aged one to three years. Habitual intakes of nutrients were evaluated according to recommendations set by the Dutch Health Council. Specific food groups were evaluated according to the Dutch food-based dietary guidelines. For most nutrients, intakes were estimated to be adequate. High intakes were found for saturated fatty acids, retinol, iodine, copper, zinc, and sodium. No statement could be provided on the adequacy of intakes of alpha-linoleic acids, N-3 fish fatty acids, fiber, and iron. 74% of the toddlers used dietary supplements, and 59% used vitamin D supplements specifically. Total median intakes of vegetables, bread, and milk products were sufficient. Consumption of bread, potatoes and cereals, milk products, fats, and drinks consisted largely of unhealthy products. Consumption of unfavorable products may have been the cause of the observed high and low intakes of several nutrients. Shifting towards a healthier diet that is more in line with the guidelines may positively affect the dietary intake of Dutch toddlers and prevent negative health impacts, also later in life.

scholarly journals Stimulated Suicidal Erythrocyte Death in Arteritis

2016 ◽  
Vol 39 (3) ◽  
pp. 1068-1077 ◽  
Author(s):  
Rosi Bissinger ◽  
Daniela S. Kempe-Teufel ◽  
Sabina Honisch ◽  
Syed M. Qadri ◽  
Elko Randrianarisoa ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Healthy Volunteers ◽  
Annexin V ◽  
Vascular Occlusion ◽  
Vascular Wall ◽  
Cellular Mechanisms ◽  
Forward Scatter ◽  
Erythrocyte Surface ◽  
Theory Result ◽  
And Oxidative Stress

Background/Aims: Arteritis is an inflammatory disease of the vascular wall leading to ischemia and vascular occlusion. Complications of arteritis include anemia, which could, at least in theory, result from suicidal erythrocyte death or eryptosis, which is characterized by erythrocyte shrinkage and phosphatidylserine (PS) exposure at the erythrocyte surface. Cellular mechanisms involved in the stimulation of eryptosis include increased cytosolic Ca2+-concentration ([Ca2+]i), oxidative stress and ceramide formation. The present study explored whether and how arteritis influences eryptosis. Methods: Blood was drawn from patients suffering from arteritis (n=17) and from healthy volunteers (n=21). PS exposure was estimated from annexin V-binding, erythrocyte volume from forward scatter, [Ca2+]i from Fluo3-fluorescence, reactive oxygen species (ROS) from DCFDA fluorescence and ceramide abundance from FITC-conjugated antibody binding in flow cytometry. The patients suffered from anemia despite 2.8±0.4% reticulocytes. Results: The percentage of PS-exposing erythrocytes was significantly higher in patients (1.1±0.1%) than in healthy volunteers (0.3±0.1%). The increase in PS exposure was paralleled by increase in oxidative stress and [Ca2+]i but not by significant changes of ceramide abundance. Erythrocyte PS exposure and ROS production were significantly enhanced in erythrocytes exposed to patient plasma as compared to exposure to plasma from healthy volunteers. Conclusion: Arteritis is associated with enhanced eryptosis due to increased [Ca2+]i and oxidative stress. The eryptosis contributes to or even accounts for the anemia in those patients. As eryptotic erythrocytes adhere to endothelial cells of the vascular wall, they could impede microcirculation and thus contribute to vascular occlusion.

scholarly journals Hydrogen-Generating Silica Material Prevents UVA-Ray-Induced Cellular Oxidative Stress, Cell Death, Collagen Loss and Melanogenesis in Human Cells and 3D Skin Equivalents

Antioxidants ◽  
2021 ◽  
Vol 10 (1) ◽  
pp. 76
Author(s):  
Li Xiao ◽  
Mai Mochizuki ◽  
Taka Nakahara ◽  
Nobuhiko Miwa
Keyword(s):  
Oxidative Stress ◽  
Cell Death ◽  
Annexin V ◽  
Human Keratinocytes ◽  
Absorption Capacity ◽  
Human Cells ◽  
Skin Equivalents ◽  
Type Iv ◽  
Silica Material ◽  
3D Skin

Ultraviolet-A (UVA) irradiation induces harmful effects on skin cells and accelerates skin aging through oxidative stress. In this study, the effects of a hydrogen-generating silica material named ULH-002 against UVA injuries in human cells and 3D skin equivalents were investigated. The oxygen radical absorption capacity (ORAC) assay showed that both freshly prepared ULH-002 solutions and 7-day-old solutions exhibited equal peroxyl radical (ROO·) scavenging activities concentration-dependently. CellROX® green/orange staining showed that ULH-002 could reduce UVA-induced oxidative stress in human keratinocytes HaCaT and human gingival fibroblasts (HGFs). ULH-002 significantly prevented UVA-induced apoptotic/necrotic cell death and cell-viability decline in HGFs and keratinocytes, as shown by Annexin V/PI apoptosis assay and PrestoBlue assay, respectively. Immunostaining showed that ULH-002 prevented the UVA-induced deterioration of expression of both type IV and I collagens in the 3D skin equivalents, and similarly in monolayer HGFs. UVA-enhanced melanogenesis was observed in human melanocytes HMV-II and HMV-II cell-containing 3D skin equivalents, but markedly prevented by ULH-002 as demonstrated by Fontana–Masson’s staining. In conclusion, our data suggested that ULH-002 could protect human keratinocytes and fibroblasts from UVA-induced injuries, prevent the loss of type IV and I collagens, as well as reduce melanogenesis. ULH-002 might be developed as a skin care reagent in the cosmetic industry.

scholarly journals Can Diet Influence the COVID-19 Mortality Rate?

2020 ◽  
Vol 1 (1) ◽  
pp. 16-18
Author(s):  
Amanda Avery
Keyword(s):  
Angiotensin Converting Enzyme ◽  
Regional Differences ◽  
Dietary Habits ◽  
European Countries ◽  
Converting Enzyme ◽  
Dietary Interventions ◽  
Angiotensin Converting Enzyme Activity ◽  
Death Rates ◽  
Angiotensin Converting Enzyme 2 ◽  
The Many

Reported COVID-19 deaths in Germany are relatively low as compared to many European countries. Among the several explanations proposed, an early and large testing of the population was put forward. Most current debates on COVID-19 focus on the differences among countries, but little attention has been given to regional differences and diet. The low-death rate European countries (e.g. Austria, Baltic States, Czech Republic, Finland, Norway, Poland, Slovakia) have used different quarantine and/or confinement times and methods and none have performed as many early tests as Germany. Among other factors that may be significant are the dietary habits. It seems that some foods largely used in these countries may reduce angiotensin-converting enzyme activity or are anti-oxidants. Among the many possible areas of research, it might be important to understand diet and angiotensin-converting enzyme-2 (ACE2) levels in populations with different COVID-19 death rates since dietary interventions may be of great benefit.

scholarly journals Selected Kefir Water from Malaysia Attenuates Hydrogen Peroxide-Induced Oxidative Stress by Upregulating Endogenous Antioxidant Levels in SH-SY5Y Neuroblastoma Cells

Antioxidants ◽  
2021 ◽  
Vol 10 (6) ◽  
pp. 940
Author(s):  
Muganti Rajah Kumar ◽  
Swee Keong Yeap ◽  
Han Chung Lee ◽  
Nurul Elyani Mohamad ◽  
Muhammad Nazirul Mubin Aziz ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Hydrogen Peroxide ◽  
Neuroblastoma Cells ◽  
Annexin V ◽  
Morphological Features ◽  
Lower Percentage ◽  
Total Phenolic ◽  
Neuroprotective Effects ◽  
Antioxidant Power ◽  
Pre Treatment

Kefir, a fermented probiotic drink was tested for its potential anti-oxidative, anti-apoptotic, and neuroprotective effects to attenuate cellular oxidative stress on human SH-SY5Y neuroblastoma cells. Here, the antioxidant potentials of the six different kefir water samples were analysed by total phenolic content (TPC), total flavonoid content (TFC), ferric reducing antioxidant power (FRAP), and 2,2′-diphenyl-1-picrylhydrazyl radical (DPPH) assays, whereas the anti-apoptotic activity on hydrogen peroxide (H2O2) induced SH-SY5Y cells was examined using MTT, AO/PI double staining, and PI/Annexin V-FITC assays. The surface and internal morphological features of SH-SY5Y cells were studied using scanning and transmission electron microscopy. The results indicate that Kefir B showed the higher TPC (1.96 ± 0.54 µg GAE/µL), TFC (1.09 ± 0.02 µg CAT eq/µL), FRAP (19.68 ± 0.11 mM FRAP eq/50 µL), and DPPH (0.45 ± 0.06 mg/mL) activities compared to the other kefir samples. The MTT and PI/Annexin V-FITC assays showed that Kefir B pre-treatment at 10 mg/mL for 48 h resulted in greater cytoprotection (97.04%), and a significantly lower percentage of necrotic cells (7.79%), respectively. The Kefir B pre-treatment also resulted in greater protection to cytoplasmic and cytoskeleton inclusion, along with the conservation of the surface morphological features and the overall integrity of SH-SY5Y cells. Our findings indicate that the anti-oxidative, anti-apoptosis, and neuroprotective effects of kefir were mediated via the upregulation of SOD and catalase, as well as the modulation of apoptotic genes (Tp73, Bax, and Bcl-2).

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