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

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.

Agronomy ◽  
2021 ◽  
Vol 11 (7) ◽  
pp. 1414
Author(s):  
Uroš Čakar ◽  
Mirjana Čolović ◽  
Danijela Milenković ◽  
Branislava Medić ◽  
Danijela Krstić ◽  
...  

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.


2006 ◽  
Vol 84 (10) ◽  
pp. 1071-1079 ◽  
Author(s):  
Farong Yu ◽  
Shunqing Lu ◽  
Fahong Yu ◽  
Shutao Feng ◽  
Peter M. McGuire ◽  
...  

The present study examined the effects of derivatives of galactosides and glucosides in a polysaccharide extract from Euphorbia kansui (Euphorbiaceae) on exercise-induced oxidative stress in mice. Exhaustive swimming exercise significantly increases the degree of lipid peroxidation in terms of malondialdehyde content and reduces the antioxidant activities of superoxide dismutase (SOD) and glutathione peroxidase (GPx). Our findings revealed that chronic oral treatment with the extract elevates enzymatic activities of SOD and GPx accompanied by a corresponding decrease in malondialdehyde. The antioxidative activities of these compounds against exercise-induced oxidative stress are correlated with various activities such as reducing the production of superoxide and hydroxyl radicals, inhibiting lipid peroxidation, enhancing antioxidative defenses, and increasing the production of SOD and GPx activity and expression in different tissues. These compounds may be involved in glycogen metabolism to meet the requirement of working skeletal muscles and act as antioxidants by terminating the chain reaction of lipid peroxidation to maintain the morphological stability of mitochondria in spinal motor neurons. These observations suggest that E. kansui has antioxidative and antifatigue properties and can be given as prophylactic and (or) therapeutic supplements for increasing antioxidant enzyme activities and preventing lipid peroxidation during strenuous exercise.


2015 ◽  
Vol 36 (3) ◽  
pp. 966-979 ◽  
Author(s):  
Hao Liu ◽  
Ping Mao ◽  
Jia Wang ◽  
Tuo Wang ◽  
Chang-Hou Xie

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.


F1000Research ◽  
2019 ◽  
Vol 8 ◽  
pp. 1067 ◽  
Author(s):  
Faith A. Kwa ◽  
Nabeela K. Dulull ◽  
Ute Roessner ◽  
Daniel A. Dias ◽  
Thusitha W. Rupasinghe

Background: Age-related macular degeneration (AMD) is a leading cause of blindness in the ageing population. Without effective treatment strategies that can prevent disease progression, there is an urgent need for novel therapeutic interventions to reduce the burden of vision loss and improve patients’ quality of life. Dysfunctional innate immune responses to oxidative stress observed in AMD can be caused by the formation of oxidised lipids, whilst polyunsaturated fatty acids have shown to increase the risk of AMD and disease progression in affected individuals. Previously, our laboratory has shown that the vegetable-derived isothiocyanate, L-sulforaphane (LSF), can protect human adult pigment epithelial cells from oxidative damage by upregulating gene expression of the oxidative stress enzyme Glutathione-S-Transferase µ1. This study aims to validate the protective effects of LSF on human retinal cells under oxidative stress conditions and to reveal the key players in fatty acid and lipid metabolism that may facilitate this protection. Methods: The in vitro oxidative stress model of AMD was based on the exposure of an adult retinal pigment epithelium-19 cell line to 200µM hydrogen peroxide. Percentage cell proliferation following LSF treatment was measured using tetrazolium salt-based assays. Untargeted fatty acid profiling was performed by gas chromatography-mass spectrometry. Untargeted lipid profiling was performed by liquid chromatography-mass spectrometry. Results: Under hydrogen peroxide-induced oxidative stress conditions, LSF treatment induced dose-dependent cell proliferation. The key fatty acids that were increased by LSF treatment of the retinal cells include oleic acid and eicosatrienoic acid. LSF treatment also increased levels of the lipid classes phosphatidylcholine, cholesteryl ester and oxo-phytodienoic acid but decreased levels of phosphatidylethanolamine lipids. Conclusions: We propose that retinal cells at risk of oxidative damage and apoptosis can be pre-conditioned with LSF to regulate levels of selected fatty acids and lipids known to be implicated in the pathogenesis and progression of AMD.


2019 ◽  
Vol 13 (1) ◽  
pp. 37-44 ◽  
Author(s):  
Margarita Velásquez ◽  
Darío Méndez ◽  
Carlos Moneriz

Background: Pyridoxine has reduction and prevention against the levels of reactive oxygen species in in vitro studies. However, the biochemical mechanism that explains this behavior has not yet been fully clarified. Objective: To evaluate the effect of pyridoxine against oxidative damage on the membrane of human erythrocytes. Methods: Cumene hydroperoxide was used to induce oxidative stress in protein and lipid. Human erythrocytes were incubated with pyridoxine and cumene hydroperoxide, either alone or together for 8 h. Oxidative damage was determined by measuring lipid peroxidation and membrane protein carbonylation. Results: The results indicate that the malondialdehyde concentration decreased with increasing concentration of pyridoxine. The membrane protein content also decreased with increasing concentration of vitamin B6, which was confirmed by the decreased signal intensity in the western blot when compared to control without pyridoxine. Results demonstrate that pyridoxine can significantly decrease lipid peroxidation and protein carbonylation in red cell membrane exposed to high concentrations of oxidant agent. Conclusion: Pyridoxine showed a protective effect against the oxidative stress in human erythrocytes in vitro, inhibiting the carbonylation and the oxidative damage of erythrocyte membrane proteins. To date, such an effect has not yet been reported in terms of protein oxidation.


Molecules ◽  
2019 ◽  
Vol 24 (18) ◽  
pp. 3322 ◽  
Author(s):  
Daofeng Qu ◽  
Chu Liu ◽  
Mengxue Jiang ◽  
Lifang Feng ◽  
Yuewen Chen ◽  
...  

Some studies have demonstrated that acrylamide (AA) was correlated with oxidative stress, resulting in physical damage. The jackfruit flake was an immature pulp that contained a high level of antioxidant activity. This study aimed to assess the defensive efficacy of jackfruit flake in AA-induced oxidative stress before and after simulated gastrointestinal digestion. Our results indicate that the total polyphenol content of Jackfruit flake digest (Digestive products of jackfruit flake after gastrointestinal, JFG) was diminished; however, JFG had raised the relative antioxidant capacity compared to Jackfruit flake extract (JFE). Additionally, the results of High Performance Liquid Chromatography-Mass Spectrometry (HPLC-MS) implied that a proportion of compounds were degraded/converted into other unknown and/or undetected metabolites. Further, by high content analysis (HCA) techniques, JFG markedly reduced cytotoxicity and excessive production of reactive oxygen species (ROS) in cells, thereby alleviating mitochondrial disorders. In this study, it may be converted active compounds after digestion that had preferable protective effects against AA-induced oxidative damage.


2020 ◽  
Vol 16 (3) ◽  
pp. 284-293
Author(s):  
George Laylson da Silva Oliveira ◽  
Maria das Dores Alves de Oliveira ◽  
Maria da Conceição Oliveira Prado ◽  
Alexandre de Barros Falcão Ferraz ◽  
José Carlos Correia Lima da Silva ◽  
...  

Background: Garcinielliptone FC corresponds to a polyprenylated acylphloroglucinol having a benzophenonic core (diphenylmethanone) substituted with isoprenyl(s) group(s) (3-methyl-2-butenyl) and 2-isopropenyl-hex-5-enyl. Objective: The present work evaluated the antioxidant activity of garcinielliptone FC (GFC) in vitro against non-biological radicals [2,2-diphenyl-1-picrylhydrazyl (DPPH•) and 2,2'-azinobis-3- ethylbenzothiazoline-6-sulfonic acid (ABTS•+)] and ex vivo against oxidative damage induced by AAPH (2,2'-azobis-2-methylpropionamidine dihydrochloride) and iron/citrate ion in erythrocytes and mitochondria, respectively. Methods: In addition to the protective effect, the main biochemical indexes of oxidative stress, such as lipid peroxidation through the formation of Thiobarbituric Acid Reactive Substances (TBARS), Superoxide Dismutase (SOD), Catalase (CAT) activity and reduced glutathione (GSH) levels. Results: According to the results obtained in erythrocytes, the antioxidant results at concentrations of 0.1, 0.3, 0.7, 1.5 and 3.0 mM were 26.34 ± 0.68, 43.39 ± 2.17, 62.27 ± 2.17, 86.69 ± 0.47 and 92.89 ± 0.45%, respectively, where GFC reduced the rate of oxidative hemolysis when compared to AAPH (p<0.05). The antioxidant activity observed in erythrocytes was also seen in mitochondria in which GFC reduced mitochondrial swelling by increasing the absorbance when compared to iron/citrate ion complex (p<0.05). In both biological models, GFC had an antioxidant effect on erythrocyte and mitochondrial redox balance when analyzing oxidative stress biomarkers, such as reduction of lipid peroxidation and inhibition of depletion in the activity of SOD, CAT and GSH levels. Conclusion: In conclusion, GFC had in vitro and ex vivo antioxidant activity against oxidative damage induced in erythrocytes and mitochondria acting on the erythrocytic and mitochondrial redox balance.


2009 ◽  
Vol 25 (8) ◽  
pp. 545-550 ◽  
Author(s):  
Ismail Karabulut ◽  
Z. Dicle Balkanci ◽  
Bilge Pehlivanoglu ◽  
Aysen Erdem ◽  
Ersin Fadillioglu

Toluene, an organic solvent used widely in the industry, is highly lipophilic and accumulates in the cell membrane impeding transport through it. Its metabolites cause oxygen radical formation that react with unsaturated fatty acids and proteins in erythrocytes leading to lipid peroxidation and protein breakdown. In this study, we aimed to investigate the membrane stabilizing and the oxidative stress—inducing effects of toluene in human erythrocytes. Measurements of osmotic fragility, mean corpuscular volume (MCV), oxidative stress parameters and antioxidant enzyme activities were performed simultaneously both in individuals exposed to toluene professionally (in vivo) and human erythrocytes treated with toluene (in vitro). To measure osmotic fragility, erythrocytes were placed in NaCl solutions at various concentrations (0.1% [blank], 0.38%, 0.40%, 0.42%, 0.44%, 0.46%, 0.48% and 1% [stock]). Percentage of haemolysis in each solution was calculated with respect to the 100% haemolysis in the blank solution. The erythrocyte packs prepared at the day of the above-mentioned measurements were kept at —80°C until the time for determination of malonyldialdehyde and protein carbonyl levels, and catalase (CAT) and glutathione peroxidase activities as indicators of oxidative stress. Toluene increased oxidative stress parameters significantly both in vivo and in vitro; it also caused a significant decrease in the activities of antioxidant enzymes. Osmotic fragility was altered only in the case of in vitro exposure. In conclusion, toluene exposure resulted in increased lipid peroxidation and protein damage both in vivo and in vitro. Although, it is natural to expect increased osmotic fragility due to oxidative properties of toluene, its membrane-stabilizing effect overcame the oxidative properties leading to decreased osmotic fragility or preventing its deterioration in vitro and in vivo toluene exposures, respectively, in the present study.


2019 ◽  
Vol 2019 ◽  
pp. 1-15 ◽  
Author(s):  
Wattanased Jarisarapurin ◽  
Wariya Sanrattana ◽  
Linda Chularojmontri ◽  
Khwandow Kunchana ◽  
Suvara K. Wattanapitayakul

It has been proven that high consumption of fruit and vegetable lowers the risks of cardiovascular and other oxidative stress-related diseases. Here we evaluated the effects of a tropical fruit, unripeCarica papaya(UCP), on endothelial protection against oxidative damage induced by H2O2. The antioxidant properties of UCP were investigated using the assays of FRAP and ORAC and specific ROS scavenging activities (H2O2,O2•-, OH•, HOCl). Cytoprotective property was tested in human endothelial cell line EA.hy926 with respect to cell survival, intracellular ROS levels, antioxidant enzyme activities (CAT, SOD, GPX), survival/stress signaling (AKT, JNK, p38), and nuclear signaling (Nrf2, NF-kB). UCP processed high antioxidant activity and scavenging activity against H2O2> OH•>O2•-> HOCl, respectively. UCP improved cell survival in the milieu of ROS reduction. While SOD was increased by UCP, CAT activity was enhanced when cells were challenged with H2O2. UCP had no impact on H2O2-activated AKT, JNK, and p38 signaling but significantly decreased nuclear NF-κB levels. The overactivation of Nrf2 in response to oxidative stress was constrained by UCP. In conclusion, UCP protected endothelial cells against oxidative damage through intracellular ROS reduction, enhanced CAT activity, suppression of NF-kB, and prohibition of Nrf2 dysregulation. Thus, UCP might be a candidate for development of nutraceuticals against CVD and oxidative-related diseases and conditions.


F1000Research ◽  
2019 ◽  
Vol 8 ◽  
pp. 1067
Author(s):  
Faith A. Kwa ◽  
Nabeela K. Dulull ◽  
Ute Roessner ◽  
Daniel A. Dias ◽  
Thusitha W. Rupasinghe

Background: Age-related macular degeneration (AMD) is a leading cause of blindness in the ageing population. Without effective treatment strategies that can prevent disease progression, there is an urgent need for novel therapeutic interventions to reduce the burden of vision loss and improve patients’ quality of life. Dysfunctional innate immune responses to oxidative stress observed in AMD can be caused by the formation of oxidised lipids, whilst polyunsaturated fatty acids have shown to increase the risk of AMD and disease progression in affected individuals. Previously, our laboratory has shown that the vegetable-derived isothiocyanate, L-sulforaphane (LSF), can protect human adult pigment epithelial cells from oxidative damage by upregulating gene expression of the oxidative stress enzyme Glutathione-S-Transferase µ1. This study aims to validate the protective effects of LSF on human retinal cells under oxidative stress conditions and to reveal the key players in fatty acid and lipid metabolism that may facilitate this protection. Methods: The in vitro oxidative stress model of AMD was based on the exposure of an adult retinal pigment epithelium-19 cell line to 200µM hydrogen peroxide. Percentage cell proliferation following LSF treatment was measured using tetrazolium salt-based assays. Untargeted fatty acid profiling was performed by gas chromatography-mass spectrometry. Untargeted lipid profiling was performed by liquid chromatography-mass spectrometry. Results: Under hydrogen peroxide-induced oxidative stress conditions, LSF treatment induced dose-dependent cell proliferation. The key fatty acids that were increased by LSF treatment of the retinal cells include oleic acid and eicosatrienoic acid. LSF treatment also increased levels of the lipid classes phosphatidylcholine, cholesteryl ester and oxo-phytodienoic acid but decreased levels of phosphatidylethanolamine lipids. Conclusions: We propose that retinal cells at risk of oxidative damage and apoptosis can be pre-conditioned with LSF to regulate levels of selected fatty acids and lipids known to be implicated in the pathogenesis and progression of AMD.


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