Activation of Nrf2-driven antioxidant enzymes by cardamonin confers neuroprotection of PC12 cells against oxidative damage

2017 ◽  
Vol 8 (3) ◽  
pp. 997-1007 ◽  
Author(s):  
Shoujiao Peng ◽  
Yanan Hou ◽  
Juan Yao ◽  
Jianguo Fang
Keyword(s):  
Oxidative Stress ◽  
Antioxidant Enzymes ◽  
Free Radicals ◽  
Oxidative Damage ◽  
Pc12 Cells ◽  
Redox Equilibrium

Oxidative stress represents a disorder of the redox equilibrium between the production of free radicals and the capability of cells to eliminate them.

scholarly journals Exercise protects against doxorubicin-induced oxidative stress and proteolysis in skeletal muscle

2011 ◽  
Vol 110 (4) ◽  
pp. 935-942 ◽  
Author(s):  
Ashley J. Smuder ◽  
Andreas N. Kavazis ◽  
Kisuk Min ◽  
Scott K. Powers
Keyword(s):  
Oxidative Stress ◽  
Skeletal Muscle ◽  
Antioxidant Enzymes ◽  
Heat Shock ◽  
Heat Shock Protein ◽  
Oxidative Damage ◽  
Muscle Fibers ◽  
Muscular Exercise ◽  
Protease Activation ◽  
Exercise Induced

Doxorubicin (Dox) is a potent antitumor agent used in cancer treatment. Unfortunately, Dox is myotoxic and results in significant reductions in skeletal muscle mass and function. Complete knowledge of the mechanism(s) by which Dox induces toxicity in skeletal muscle is incomplete, but it is established that Dox-induced toxicity is associated with increased generation of reactive oxygen species and oxidative damage within muscle fibers. Since muscular exercise promotes the expression of numerous cytoprotective proteins (e.g., antioxidant enzymes, heat shock protein 72), we hypothesized that muscular exercise will attenuate Dox-induced damage in exercise-trained muscle fibers. To test this postulate, Sprague-Dawley rats were randomly assigned to the following groups: sedentary, exercise, sedentary with Dox, or exercise with Dox. Our results show increased oxidative stress and activation of cellular proteases (calpain and caspase-3) in skeletal muscle of animals treated with Dox. Importantly, our findings reveal that exercise can prevent the Dox-induced oxidative damage and protease activation in the trained muscle. This exercise-induced protection against Dox-induced toxicity may be due, at least in part, to an exercise-induced increase in muscle levels of antioxidant enzymes and heat shock protein 72. Together, these novel results demonstrate that muscular exercise is a useful countermeasure that can protect skeletal muscle against Dox treatment-induced oxidative stress and protease activation in skeletal muscles.

Oxidative Stress, Mitochondrial DNA Mutation, and Impairment of Antioxidant Enzymes in Aging

2002 ◽  
Vol 227 (9) ◽  
pp. 671-682 ◽  
Author(s):  
Yau-Huei Wei ◽  
Hsin-Chen Lee
Keyword(s):  
Oxidative Stress ◽  
Mitochondrial Dna ◽  
Antioxidant Enzymes ◽  
Oxidative Damage ◽  
Large Scale ◽  
Wide Spectrum ◽  
Radical Scavenging ◽  
Mtdna Mutations ◽  
Enhanced Production ◽  
Age Related

Mitochondria do not only produce less ATP, but they also increase the production of reactive oxygen species (ROS) as byproducts of aerobic metabolism in the aging tissues of the human and animals. It is now generally accepted that aging-associated respiratory function decline can result in enhanced production of ROS in mitochondria. Moreover, the activities of free radical-scavenging enzymes are altered in the aging process. The concurrent age-related changes of these two systems result in the elevation of oxidative stress in aging tissues. Within a certain concentration range, ROS may induce stress response of the cells by altering expression of respiratory genes to uphold the energy metabolism to rescue the cell. However, beyond the threshold, ROS may cause a wide spectrum of oxidative damage to various cellular components to result in cell death or elicit apoptosis by induction of mitochondrial membrane permeability transition and release of apoptogenic factors such as cytochrome c. Moreover, oxidative damage and large-scale deletion and duplication of mitochondrial DNA (mtDNA) have been found to increase with age in various tissues of the human. Mitochondria act like a biosensor of oxidative stress and they enable cell to undergo changes in aging and age-related diseases. On the other hand, it has recently been demonstrated that impairment in mitochondrial respiration and oxidative phosphorylation elicits an increase in oxidative stress and causes a host of mtDNA rearrangements and deletions. Here, we review work done in the past few years to support our view that oxidative stress and oxidative damage are a result of concurrent accumulation of mtDNA mutations and defective antioxidant enzymes in human aging.

scholarly journals Advances on antioxidants in research and applications

2019 ◽  
Vol 131 ◽  
pp. 01009
Author(s):  
Ruirui Song ◽  
Qi Wu ◽  
Lin Zhao ◽  
Zhenyu Yun
Keyword(s):  
Oxidative Stress ◽  
Free Radicals ◽  
Chronic Diseases ◽  
Significant Role ◽  
Human Body ◽  
Relevant Research ◽  
Redox Equilibrium ◽  
Practical Applications ◽  
Existing Problems ◽  
Prevention And Treatment

Antioxidants play a significant role in the prevention and treatment of numerous chronic diseases as they prevent oxidative stress and maintain reduction-oxidation (redox) equilibrium in the human body by eliminating reactive free radicals effectively. This study focused on the types and applications of antioxidants and discussed the existing problems with regard to the practical applications of antioxidants. Also, it presented a review of the latest research on antioxidants in China and abroad and performed a comprehensive, objective analysis of relevant research on antioxidants.

Hydrophobicity of whey protein hydrolysates enhances the protective effect against oxidative damage on PC 12 cells

2014 ◽  
Vol 82 (1) ◽  
pp. 1-7 ◽  
Author(s):  
Qiu-Xiang Zhang ◽  
Man-Man Jin ◽  
Li Zhang ◽  
Hui-Xin Yu ◽  
Zhen Sun ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Oxidative Damage ◽  
Protective Effect ◽  
Pc12 Cells ◽  
Whey Protein ◽  
Protein Hydrolysates ◽  
Antioxidant Ability ◽  
Ability Test ◽  
Whey Protein Hydrolysates ◽  
Three Components

The relationship between hydrophobicity and the protective effect of whey protein hydrolysates (WPHs) against oxidative stress was studied. Whey protein was first hydrolysed by pepsin and trypsin to obtain WPHs. After absorbed by macroporous adsorption resin DA201-C, three fractions named as M20, M40, and M60 were eluted by various concentrations of ethanol. The hydrophobicity showed a trend of increase from M20 to M60. Antioxidant ability test in vitro indicated that all the three components of WPHs displayed reasonably good antioxidant ability. Moreover, with the increase of hydrophobicity, antioxidant ability of WPHs improved significantly. Then rat pheochromocytoma line 12 (PC12) cells oxidative model was built to evaluate the suppression of oxidative stress of three components on PC12 cells induced by H2O2. Morphological alterations, cell viability, apoptosis rate, and intracellular antioxidase system tests all indicated that WPHs exert significant protection on PC cells against H2O2-induced damage. Among them, M60 had the highest protective effect by increasing 19·3% cell survival and reducing 28·6% cell apoptosis. These results suggested hydrophobicity of WPHs was contributing to the antioxidant ability and the protective effect against oxidative damage.

scholarly journals Pechiche (Vitex cymosa Berteo ex Speng), a Nontraditional Fruit from Ecuador, is a Dietary Source of Phenolic Acids and Nutrient Minerals, in Addition to Efficiently Counteracting the Oxidative-Induced Damage in Human Dermal Fibroblasts

Antioxidants ◽  
2020 ◽  
Vol 9 (2) ◽  
pp. 109
Author(s):  
Mabel Guevara ◽  
Luis A. Valdés-Silverio ◽  
María G. Granda-Albuja ◽  
Gabriel Iturralde ◽  
Tatiana Jaramillo-Vivanco ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Antioxidant Enzymes ◽  
Oxidative Damage ◽  
Phenolic Acids ◽  
Glutathione Transferase ◽  
Dermal Fibroblasts ◽  
Human Dermal Fibroblasts ◽  
Atp Levels ◽  
Intracellular Ros ◽  
Phosphorus And Potassium

Pechiche fruits (Vitex cymosa Berteo ex Speng) from Ecuador were studied to determine their phenolic acid profile, nutrient minerals and capacity to protect primary human dermal fibroblasts (HDFa) against oxidative-induced damage. Up to five phenolic acids were identified, with homovanillic acid as the main one. Vitamin C, β-carotene and lutein were also determined. Phosphorus and potassium were the main macrominerals, while iron was the principal micromineral. HDFa were preincubated with a crude pechiche extract (PCext) and then subjected to oxidative stress. The activity of five antioxidant enzymes, intracellular reactive oxygen species (ROS) and ATP levels and lipid peroxidation and protein oxidation were used as markers of oxidative damage. Preincubation with PCext for 24 h allowed for the significant reduction of intracellular ROS levels, improved the intracellular ATP levels and protected lipids and proteins against oxidative damage (p < 0.05). Additionally, preincubation with PCext was also able to significantly (p < 0.05) improve the activity of the antioxidant enzymes catalase, superoxide dismutase, glutathione peroxidase, glutathione reductase and glutathione transferase, compared to the stressed group without pretreatment. The results obtained in this study suggest the potential of pechiche as a source of bioactive compounds, as well as its beneficial effect against oxidative stress.

523. PLACENTAL ANTIOXIDANT ENZYMES IN RAT PREGNANCY SHOW ZONE- AND STAGE-DEPENDENT VARIATION

2009 ◽  
Vol 21 (9) ◽  
pp. 122
Author(s):  
M. L. Jones ◽  
P. J. Mark ◽  
T. A. Mori ◽  
B. J. Waddell
Keyword(s):  
Oxidative Stress ◽  
Antioxidant Enzymes ◽  
Oxidative Damage ◽  
Mrna Expression ◽  
Late Pregnancy ◽  
Late Gestation ◽  
Ros Generation ◽  
Dexamethasone Treatment ◽  
Endogenous Protection ◽  
Thioredoxin Reductases

Placental oxidative stress plays a key role in the pathophysiology of placenta-related disorders including preeclampsia. Protection from oxidative stress is provided by antioxidant enzymes which inactivate reactive oxygen species (ROS). The rat placenta consists of two major zones, the junctional (JZ) and labyrinth (LZ), and because only the LZ grows in late gestation we hypothesized it generates more ROS and thus requires greater antioxidant protection. Our previous studies on expression of the antioxidants superoxide dismutase (SOD)-1, SOD-2 and catalase support this hypothesis. Here, we extend these observations to include mRNA expression of SOD-3 and thioredoxin reductases (Txnrd-1, -2, -3) and activities of SOD, hydrogen peroxide (H2O2) scavenging and xanthine oxidase (XO). Placental oxidative damage was assessed by measurement of F2-isoprostanes and TBARS concentrations. We also measured the effects of maternal dexamethasone treatment, since glucocorticoid excess is known to induce oxidative damage in other tissues. Placentas were collected from untreated mothers on days 16 and 22 (term=day 23) and on day 22 after dexamethasone treatment from day 13 (1 μg/ml drinking water). SOD-3, Txnrd-1, -2, and -3 mRNAs were measured in JZ and LZ by qRT-PCR. F2-isoprostanes were measured by GC-MS and kit assays were used to measure TBARS and the activities of SOD, H2O2 scavenging and XO. In both placental zones, expression of SOD-3 and Txnrd-1 mRNAs and H2O2 scavenging activity decreased from day 16 to 22, whereas XO activity increased. Dexamethasone treatment increased H2O2 scavenging in both zones, but had no effect on SOD or XO activities or antioxidant mRNA expression. Despite predicted increases in placental ROS generation in late pregnancy and after dexamethasone, neither F2-isoprostanes nor TBARS were increased. These and our previous data suggest that endogenous protection against oxidative stress is abundant in the rat placenta and provides protection against potential oxidative insults including glucocorticoid excess.

scholarly journals Timing the evolution of antioxidant enzymes in cyanobacteria

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Joanne S. Boden ◽  
Kurt O. Konhauser ◽  
Leslie J. Robbins ◽  
Patricia Sánchez-Baracaldo
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Superoxide Dismutase ◽  
Antioxidant Enzymes ◽  
Free Radicals ◽  
Molecular Oxygen ◽  
Molecular Clocks ◽  
Oxygen Species ◽  
Terrestrial Habitats ◽  
Iron Nickel

AbstractThe ancestors of cyanobacteria generated Earth’s first biogenic molecular oxygen, but how they dealt with oxidative stress remains unconstrained. Here we investigate when superoxide dismutase enzymes (SODs) capable of removing superoxide free radicals evolved and estimate when Cyanobacteria originated. Our Bayesian molecular clocks, calibrated with microfossils, predict that stem Cyanobacteria arose 3300–3600 million years ago. Shortly afterwards, we find phylogenetic evidence that ancestral cyanobacteria used SODs with copper and zinc cofactors (CuZnSOD) during the Archaean. By the Paleoproterozoic, they became genetically capable of using iron, nickel, and manganese as cofactors (FeSOD, NiSOD, and MnSOD respectively). The evolution of NiSOD is particularly intriguing because it corresponds with cyanobacteria’s invasion of the open ocean. Our analyses of metalloenzymes dealing with reactive oxygen species (ROS) now demonstrate that marine geochemical records alone may not predict patterns of metal usage by phototrophs from freshwater and terrestrial habitats.

The Effects of Moderate, Strenuous, and Overtraining on Oxidative Stress Markers and DNA Repair in Rat Liver

2005 ◽  
Vol 30 (2) ◽  
pp. 186-195 ◽  
Author(s):  
Helga Ogonovszky ◽  
Maria Sasvári ◽  
Agoston Dosek ◽  
István Berkes ◽  
Takao Kaneko ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Lipid Peroxidation ◽  
Antioxidant Enzymes ◽  
Oxidative Damage ◽  
Rat Liver ◽  
Nuclear Dna ◽  
Activity Levels ◽  
Carbonyl Derivative ◽  
Stress Markers ◽  
Cell Extracts

Physical exercise above a certain load has been suggested as being a cause of oxidative stress. We have tested whether training with moderate (MT), strenuous (ST), or over (OT) load can cause alterations in the activities of antioxidant enzymes, lipid peroxidation, protein oxidation, DNA damage, or activity of 8-oxoG-DNA glycosylase (OGG1) in rat liver. The levels of corticosterone decreased in all exercising groups but the differences were not significant. Adrenocorticotrophin hormone (ACTH) levels decreased, not significantly, in MT and OT compared to C. Activity levels of antioxidant enzymes did not change significantly in the liver. The levels of reactive carbonyl derivative (RCD) content decreased in the liver of exercising animals, and the differences reached significance between control and moderately trained groups. The changes in the levels of lipid peroxidation (LIPOX) were not significant, but were lower in the exercised groups. The 8-hydroxydeoxyguanosine (8-OHdG) levels increased in the OT group, and the activity of OGG1 measured from crude cell extracts tended to increase in MT and ST. The findings of this study imply that overtraining induces oxidative damage to nuclear DNA, but not to liver lipids and proteins. Key words: exercise, oxidative damage, adaptation, OGG1

Protective Effect on Oxidative Stress Injury of Xiongma Dripping Pills Containing Serum on PC12 Cells

2014 ◽  
Vol 955-959 ◽  
pp. 744-747
Author(s):  
Lin Liu ◽  
Jia Yi Xia ◽  
Ju Huo ◽  
Zhao Ying
Keyword(s):  
Oxidative Stress ◽  
Plasma Concentration ◽  
Oxidative Damage ◽  
Protective Effect ◽  
Pc12 Cells ◽  
Dose Group ◽  
Dose Effect ◽  
Cell Culture Supernatant ◽  
Stress Injury ◽  
Oxidative Stress Injury

Object: The antioxidant dose-effect relationship and the mechanism of Xiongma Dripping Pills were study to explore the protective effects of oxidative damage in PC12 cells of different doses of Xiongma Dripping Pills containing serum. Method: Oxidative stress injury model of PC12 cells was established by peroxide hydrogen (H2O2), sodium nitroprusside (SNP), content and cell culture supernatant lactate dehydrogenase (LDH) and the liquid content of glutathione peroxidase (GSH-PX) were detected by chemical colorimetric determination. Results: There was a plasma concentration peaked in Xiongma Dripping Pills 8 times (6g•kg-1) dose group, ferulic acid plasma concentration was 10.59 ± 2.92, the plasma concentration gastrodin 18.13 ± 4.63. H2O2 and SNP could cause injury in PC12 cells, and increased LDH leakage, reduce the content of GSH-PX (P<0.01). Gung Ma the Dripping Pills can reduce LDH leakage, increase the content of GSH-PX. Xiongma Dripping Pills 8-fold dose group content is the most significant.Conclusion: There was a significant protective effect on Xiongma Dripping Pills serum containing H2O2 and SNP induced oxidative damage of PC12 cells and its mechanism was relevant with clearing the free radicals, enhanceing antioxidant enzyme activity in vivo. There was the most significant effect on Xiongma Dripping Pills 8-fold dose group, and there was positive correlation on plasma concentration and pharmacological effects.

scholarly journals Neuroprotective Effects of Coreopsis lanceolata Flower Extract against Oxidative Stress-Induced Apoptosis in Neuronal Cells and Mice

Antioxidants ◽  
2021 ◽  
Vol 10 (6) ◽  
pp. 951
Author(s):  
Hyung Don Kim ◽  
Ji Yeon Lee ◽  
Jeong-Yong Park ◽  
Dong Hwi Kim ◽  
Min Hye Kang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Antioxidant Enzymes ◽  
Pc12 Cells ◽  
Caspase 3 ◽  
Antioxidant Activities ◽  
Neuronal Cells ◽  
Water Extract ◽  
Protective Effects ◽  
Neuroprotective Effects ◽  
Induced Apoptosis

(1) Background: Coreopsis lanceolata L. is a perennial plant of the family Asteraceae, and its flower is known to contain flavonoids with various bioactivities. We evaluated the effect of Coreopsis lanceolata L. flower (CLF) extracts on H2O2-induced oxidative stress (OS) in neuronal cells and mouse neurons. (2) Methods: The flowering part of CL was used as CLF1 (70% ethanol extract) and CLF2 (water extract), and 10 types of phenolic compounds were quantified using high-performance liquid chromatography. To evaluate the neuroprotective effects of CLF, the antioxidant activities of the extracts were measured, and the expression levels of antioxidant enzymes and proteins related to OS-induced apoptosis in neuronal cells and mouse neurons treated with the extracts were investigated. (3) Results: In the in vitro study, CLF ameliorated H2O2-induced oxidative stress and induced the expression of antioxidant enzymes in PC12 cells. Furthermore, CLF1 enhanced the expression of the Bcl-xL protein but reduced the expression of Bax and the cleavage of caspase-3. In the same manner, CLF1 showed neuroprotective effects against OS in vivo. Pretreatment with CLF1 (200 mg/kg) increased the Bcl-2 protein and decreased Bax compared with the 1-methyl-4-phenylpyridinium ion (MPP+)-treated C57BL/6 mice model group. Our results suggest that the protective effects of CLF1 on MPP+-induced apoptosis may be due to its anti-apoptotic activity, through regulating the expression of the Bcl-2 family. (4) Conclusions: CLF1 exerts neuroprotective effects against OS-induced apoptosis in PC12 cells in a Parkinson’s disease model mouse. This effect may be attributable to the upregulation of Bcl-2 protein expression, downregulation of Bax expression, and inhibition of caspase-3 activation. These data indicate that CLF may provide therapeutic value for the treatment of progressive neurodegenerative diseases.

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