scholarly journals Protective Effects of Fruit Wines against Hydrogen Peroxide—Induced Oxidative Stress in Rat Synaptosomes

Agronomy ◽  
2021 ◽  
Vol 11 (7) ◽  
pp. 1414
Author(s):  
Uroš Čakar ◽  
Mirjana Čolović ◽  
Danijela Milenković ◽  
Branislava Medić ◽  
Danijela Krstić ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Hydrogen Peroxide ◽  
Glutathione Peroxidase ◽  
Membrane Damage ◽  
Principal Component ◽  
Antioxidant Enzyme Activities ◽  
Protective Effects ◽  
Sod Activity ◽  
Black Chokeberry

This study aimed to evaluate, in vitro, the antioxidative potential of fruit wines produced from berry fruits (i.e., black chokeberry, blueberry, blackberry, and raspberry), cherry, and apple by different technological processes. For this purpose, the activities of antioxidant enzymes (catalase, glutathione peroxidase (GPx), and superoxide dismutase (SOD)) and malondialdehyde (MDA) content as a marker of membrane damage were determined in wine-treated synaptosomes with hydrogen peroxide-induced oxidative stress. All studied wines induced increased antioxidant enzyme activities and decreased MDA levels compared to hydrogen peroxide-treated synaptosomes (i.e., control). The highest SOD activity was observed in synaptosomes treated with blackberry wine (6.81 U/mg), whereas blueberry wine induced the highest catalase and glutathione peroxidase activities (0.058 U/mg and 0.017 U/mg, respectively). Black chokeberry proved to be the best in lipid peroxidation protection with the lowest MDA value (1.42 nmol/mg). Finally, principal component analysis and hierarchical cluster analysis additionally highlighted a higher antioxidant capacity of wines produced from dark-skinned fruits (i.e., blackberry, black chokeberry, and blueberry). The results suggest protective effects of the fruit wines against oxidative damage, and, accordingly, their promising application as functional food.

Protective effects of casein-derived peptide VLPVPQK against hydrogen peroxide–induced dysfunction and cellular oxidative damage in rat osteoblastic cells

2017 ◽  
Vol 36 (9) ◽  
pp. 967-980 ◽  
Author(s):  
SB Mada ◽  
S Reddi ◽  
N Kumar ◽  
S Kapila ◽  
R Kapila
Keyword(s):  
Oxidative Stress ◽  
Hydrogen Peroxide ◽  
Lipid Peroxidation ◽  
Oxidative Damage ◽  
Osteoblastic Cells ◽  
Antioxidant Enzyme Activities ◽  
Protective Agent ◽  
Protective Effects ◽  
Differentiation Markers

Oxidative stress inhibits osteoblast differentiation and function that lead to the development of osteoporosis. Casein-derived peptide VLPVPQK (PEP), a potent antioxidant, was isolated from β-casein of buffalo milk. We used an in vitro oxidative stress model induced by hydrogen peroxide (H2O2) in rat osteoblastic cells to investigate the protective effects of PEP against H2O2-induced dysfunction and oxidative damage. Cells were pretreated with PEP (50–200 ng/mL) for 2, 7 or 21 days followed by 0.3 mM H2O2 treatment for 24 h and then markers of osteogenic development, oxidative damage and apoptosis were examined. PEP significantly increased the viability and differentiation markers of osteoblast cells such as alkaline phosphatase and calcium mineralization. Moreover, PEP suppressed the production of reactive oxygen species (ROS), lipid peroxidation and ameliorated H2O2-induced reduction in glutathione, superoxide dismutase and catalase activities. In addition, PEP partially inhibited caspase-9 and-3 activities and reduced propidium iodide–positive cells. Altogether, our results demonstrated that PEP could protect rat osteoblast against H2O2-induced dysfunction and oxidative damage by reduction of ROS production, lipid peroxidation and increased antioxidant enzyme activities. Thus, our data suggest that PEP might be a valuable protective agent against oxidative stress–related diseases such as osteoporosis.

Acrylamide-induced oxidative stress in human erythrocytes

2009 ◽  
Vol 28 (10) ◽  
pp. 611-617 ◽  
Author(s):  
Betul Catalgol ◽  
Gül Özhan ◽  
Buket Alpertunga
Keyword(s):  
Oxidative Stress ◽  
Reduced Glutathione ◽  
Human Erythrocytes ◽  
Antioxidant Enzyme Activities ◽  
Total Glutathione ◽  
Sod Activity ◽  
Spectrophotometric Methods ◽  
Low Concentrations ◽  
Different Doses

Acrylamide (AA), a widely used industrial chemical, is shown to be neurotoxic, mutagenic and carcinogenic. This study was carried out to investigate the effects of different doses of AA on lipid peroxidation (LPO), haemolysis, methaemoglobin (MetHb) and antioxidant system in human erythrocytes in vitro. Erythrocyte solutions were incubated with 0.10, 0.25, 0.50 and 1.00 mM of AA at 37°C for 1 hour. At the end of the incubation, malondialdehyde (MDA), an end product of LPO, was determined by liquid chromatography (LC) while total glutathione, reduced glutathione (GSH) levels, activities of superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GSH-Px) enzymes and the rates of haemolysis and MetHb were determined by spectrophotometric methods. All of the studied concentrations of AA increased MetHb formation and SOD activity, and induced MDA formation and haemolysis due to the destruction of erythrocyte cell membrane. AA caused a decrease in the activities of GSH-Px, CAT and GSH levels. However, these effects of AA were seen only at higher concentrations than AA intake estimated for populations in many countries. We suggest that LPO process may not be involved in the toxic effects of AA in low concentrations, although the present results showed that the studied concentrations of AA exert deteriorating effects on antioxidant enzyme activities, LPO process and haemolysis.

scholarly journals Allicin Protects PC12 Cells Against 6-OHDA-Induced Oxidative Stress and Mitochondrial Dysfunction via Regulating Mitochondrial Dynamics

2015 ◽  
Vol 36 (3) ◽  
pp. 966-979 ◽  
Author(s):  
Hao Liu ◽  
Ping Mao ◽  
Jia Wang ◽  
Tuo Wang ◽  
Chang-Hou Xie
Keyword(s):  
Oxidative Stress ◽  
Mitochondrial Dysfunction ◽  
Pc12 Cells ◽  
Atp Synthesis ◽  
Ros Generation ◽  
Antioxidant Enzyme Activities ◽  
Protective Effects ◽  
Cytochrome C Release ◽  
Endogenous Antioxidant

Background: Parkinson disease (PD) is a common adult-onset neurodegenerative disorder, and PD related neuronal injury is associated with oxidative stress and mitochondrial dysfunction. Allicin, the main biologically active compound derived from garlic, has been shown to exert various anti-oxidative and anti-apoptotic activities in in vitro and in vivo studies. Methods: The present study aimed to investigate the potential protective role of allicin in an in vitro PD model induced by 6-hydroxydopamine (6-OHDA) in PC12 cells. The protective effects were measured by cell viability, decreased lactate dehydrogenase (LDH) release and flow cytometry, and the anti-oxidative activity was determined by reactive oxygen species (ROS) generation, lipid peroxidation and the endogenous antioxidant enzyme activities. Mitochondrial function in PC12 cells was detected by mitochondrial membrane potential (MMP) collapse, cytochrome c release, mitochondrial ATP synthesis, and the mitochondrial Ca2+ buffering capacity. To investigate the potential mechanism, we also measured the expression of mitochondrial biogenesis factors, mitochondrial morphological dynamic changes, as well as detected mitochondrial dynamic proteins by western blot. Results: We found that allicin treatment significant increased cell viability, and decreased LDH release and apoptotic cell death after 6-OHDA exposure. Allicin also inhibited ROS generation, reduced lipid peroxidation and preserved the endogenous antioxidant enzyme activities. These protective effects were associated with suppressed mitochondrial dysfunction, as evidenced by decreased MMP collapse and cytochrome c release, preserved mitochondrial ATP synthesis, and the promotion of mitochondrial Ca2+ buffering capacity. In addition, allicin significantly enhanced mitochondrial biogenesis and prevented fragmentation of mitochondrial network after 6-OHDA treatment. The results of western blot analysis showed that the 6-OHDA induced decrease in the expression of optic atrophy type 1 (Opa-1), increase in mitochondrial fission 1 (Fis-1) and dynamin-related protein 1 (Drp-1) were all partially revised by allicin. Conclusion: In summary, our data strongly suggested that allicin treatment can exert protective effects against PD related neuronal injury through inhibiting oxidative stress and mitochondrial dysfunction with dynamic changes.

scholarly journals Tamoxifen inhibits mitochondrial membrane damage caused by disulfiram

2017 ◽  
Vol 95 (5) ◽  
pp. 556-562 ◽  
Author(s):  
Natalia Pavón ◽  
Mabel Buelna-Chontal ◽  
Francisco Correa ◽  
Belem Yoval-Sánchez ◽  
Javier Belmont ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Hydrogen Peroxide ◽  
Cytochrome C ◽  
Mitochondrial Membrane ◽  
Membrane Damage ◽  
Mitochondrial Swelling ◽  
Protective Effects ◽  
Mitochondrial Enzyme ◽  
Inner Membrane ◽  
Antioxidant Molecule

In this work, we studied the protective effects of tamoxifen (TAM) on disulfiram (Dis)-induced mitochondrial membrane insult. The results indicate that TAM circumvents the inner membrane leakiness manifested as Ca2+ release, mitochondrial swelling, and collapse of the transmembrane electric gradient. Furthermore, it was found that TAM prevents inactivation of the mitochondrial enzyme aconitase and detachment of cytochrome c from the inner membrane. Interestingly, TAM also inhibited Dis-promoted generation of hydrogen peroxide. Given that TAM is an antioxidant molecule, it is plausible that its protection may be due to the inhibition of Dis-induced oxidative stress.

scholarly journals Protective Effects and Mechanisms of Recombinant Human Glutathione Peroxidase 4 on Isoproterenol-Induced Myocardial Ischemia Injury

2021 ◽  
Vol 2021 ◽  
pp. 1-17
Author(s):  
Chang Liu ◽  
Bozhao Li ◽  
Qi Yan ◽  
Shaopeng Niu ◽  
Yiding Zhao ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Myocardial Ischemia ◽  
Glutathione Peroxidase ◽  
In Vitro Model ◽  
Cardiomyocyte Apoptosis ◽  
Protective Effects ◽  
Stress Injury ◽  
Oxidative Stress Injury ◽  
Vitro Model

Ischemic heart disease (IHD) is a cardiovascular disease with high fatality rate, and its pathogenesis is closely related to oxidative stress. Reactive oxygen species (ROS) in oxidative stress can lead to myocardial ischemia (MI) injury in many ways. Therefore, the application of antioxidants may be an effective way to prevent IHD. In recent years, glutathione peroxidase 4 (GPx4) has received increasing attention due to its antioxidant effect. In a previous study, we used the new chimeric tRNAUTuT6 to express highly active recombinant human GPx4 (rhGPx4) in amber-less Escherichia coli. In this study, we established an isoproterenol- (ISO-) induced MI injury model in rats and an in vitro model to research the protective effect and mechanism of rhGPx4 on MI injury. The results showed that rhGPx4 could reduce the area of myocardial infarction and ameliorate the pathological injury of heart tissue, significantly reduce ISO-induced abnormalities on electrocardiogram (ECG) and cardiac serum biomarkers, protect mitochondrial function, and attenuate cardiac oxidative stress injury. In an in vitro model, the results also confirmed that rhGPx4 could inhibit ISO-induced oxidative stress injury and cardiomyocyte apoptosis. The mechanism of action of rhGPx4 involves not only the inhibition of lipid peroxidation by eliminating ROS but also keeping a normal level of endogenous antioxidant enzymes by eliminating ROS, thereby preventing oxidative stress injury in cardiomyocytes. Additionally, rhGPx4 could inhibit cardiomyocyte apoptosis through a mitochondria-dependent pathway. In short, rhGPx4, a recombinant antioxidant enzyme, can play an important role in the prevention of IHD and may have great potential for application.

Antidepressant Effects of Vaccinium bracteatum via Protection Against Hydrogen Peroxide-Induced Oxidative Stress and Apoptosis

2018 ◽  
Vol 46 (07) ◽  
pp. 1499-1518 ◽  
Author(s):  
Dool-Ri Oh ◽  
Yujin Kim ◽  
Eun-Jin Choi ◽  
Ara Jo ◽  
Jawon Shin ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Hydrogen Peroxide ◽  
Cell Death ◽  
Neuronal Damage ◽  
In Vitro Models ◽  
Monoamine Oxidase A ◽  
Protective Effects ◽  
Mao A ◽  
Anti Oxidant

The present study evaluates the anti-oxidative stress activity of Vaccinium bracteatum Thunb. fruit extract (VBFW) to identify the mechanisms responsible for its antidepressant-like effects. To evaluate the antidepressant and anti-oxidant effects of VBFW, malondialdehyde (MDA), serotonin transporter (SERT), and monoamine oxidase A (MAO-A) levels were measured in a mouse model of chronic restraint stress (CRS). The underlying mechanisms preventing oxidative stress and neuronal apoptosis were investigated using in vitro models of hydrogen peroxide (H2O[Formula: see text]-induced neuronal damage. The results showed that VBFW treatment (200[Formula: see text]mg/kg) significantly reduced MDA, SERT, and MAO-A levels in the prefrontal cortex of CRS mice. Furthermore, VBFW (30[Formula: see text][Formula: see text]g/mL) exhibited protective effects against H2O2-induced cell death via inhibition of the H2O2-induced increase in Bax and decrease in Bcl-2 levels within the mitochondria of SH-SY5Y cells. Furthermore, VBFW (10 and 30[Formula: see text][Formula: see text]g/mL) exerted protective effects against H2O2-induced cell death through inhibition of key mitochondria-associated apoptotic proteins such as cytochrome c, caspase-3 and PARP. Additionally, VBFW (10 and 30[Formula: see text][Formula: see text]g/mL) could improve the activity of anti-oxidant enzymes (such as SOD and catalase) in H2O2-treated SH-SY5Y cells. These results suggest that the antidepressant and anti-oxidant effects of VBFW might be mediated by the regulation of SERT and MAO-A, and possibly associated with regulation of oxidative stress-induced apoptosis.

Investigation of the oxidative stress condition for occupational exposure to methyl methacrylate

2016 ◽  
Vol 33 (1) ◽  
pp. 61-66 ◽  
Author(s):  
Buğra Soykut ◽  
Onur Erdem ◽  
Cemal Akay ◽  
Bülent Pişkin
Keyword(s):  
Oxidative Stress ◽  
Glutathione Peroxidase ◽  
Methyl Methacrylate ◽  
Ambient Air ◽  
Exposed Group ◽  
Control Group ◽  
Antioxidant Enzyme Activities ◽  
Sod Activity ◽  
Toxicological Effects ◽  
Significant Difference

The purpose of this study is the evaluation of possible toxicological effects on dental personnel, who are exposed to the production materials of prostheses during their entire working life. In this study, the level of methyl methacrylate (MMA) in ambient air was measured as an indicator of external exposure on the personnel. In order to evaluate the possible toxic effects of oxidative stress, which is thought to play an important role in the formation process of many diseases such as cancer, blood samples of volunteers were examined via the ultraviolet-spectroscopic determination of superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase antioxidant enzyme activities, comparing occupationally MMA-exposed ( n = 69) and control ( n = 67) groups. In these groups, malondialdehyde (MDA) and glutathione levels were also determined by the same method. The results showed that SOD activity and MDA and glutathione levels were significantly higher in the exposed group when compared with the control group ( p < 0.001). A significant decrease was determined in the glutathione peroxidase activities of the exposed group ( p < 0.05). No significant difference in CAT activities between the groups has been found. When the results obtained in the study are considered, it is suggested that an adaptive response might be developed by dental technicians against low-level MMA exposure.

Sign in / Sign up

Export Citation Format

Share Document