Photosynthetic pigments content and parameters of oxidative stress in the amaranth species with increasing water deficiency

The dynamics of the photosynthetic pigments content and parameters of oxidative stress with an increasing water deficit in the leaves of 40-days-old plants of two amaranth species - Amaranthus paniculatus L. (cv. Rubin) and Amaranthus caudatus L. (cv. Chyrvony aksamit), grown in a pot culture, was studied. Specific features of the development of water deficiency in amaranth leaves were revealed: amaranth plants Amaranthus paniculatus L. showed a stronger development of water deficit in leaves than Amaranthus caudatus L. after 4-days soil drought, which after 8 days increased in two species to 73.7 and 55.7 %, respectively. Under moderate drought, the amount of photosynthetic pigments (chlorophyll (Chl) and carotenoids) based on dry leaf weight increased in two amaranth species, but after 8 days of soil drought, the content of Chl (a + b) was reduced by 2.0-2.1 times, and carotenoids - 1.8-1.9 times relative to the physiological level. As a result of a 4-days soil drought in the leaves of Amaranthus paniculatus L., there was a significant decrease in the content of reactive oxygen species (ROS) and the activity of lipid peroxidation (LPO), while in Amaranthus caudatus L. an increase in the levels of ROS and LPO was observed. With an increase in the pressure of the stress factor in the leaves of amaranth of the two studied species, a decrease in the ROS content and LPO activity relative to physiological values was revealed. A conclusion was made about the different mechanisms of ROS generation and the flow of LPO processes at different stages of soil drought in the leaves of different amaranth species.

Download Full-text

The Roles of Environmental Factors in Regulation of Oxidative Stress in Plant

BioMed Research International ◽

10.1155/2019/9732325 ◽

2019 ◽

Vol 2019 ◽

pp. 1-11 ◽

Cited By ~ 34

Author(s):

Xiulan Xie ◽

Zhouqing He ◽

Nifan Chen ◽

Zizhong Tang ◽

Qiang Wang ◽

...

Keyword(s):

Oxidative Stress ◽

Environmental Factors ◽

Molecular Mechanisms ◽

Extreme Temperature ◽

Ultraviolet B ◽

Antioxidant Systems ◽

Ros Generation ◽

Physiological Level ◽

Nonenzymatic Antioxidants ◽

Cellular Components

Exposure to a variety of environmental factors such as salinity, drought, metal toxicity, extreme temperature, air pollutants, ultraviolet-B (UV-B) radiation, pesticides, and pathogen infection leads to subject oxidative stress in plants, which in turn affects multiple biological processes via reactive oxygen species (ROS) generation. ROS include hydroxyl radicals, singlet oxygen, and hydrogen peroxide in the plant cells and activates signaling pathways leading to some changes of physiological, biochemical, and molecular mechanisms in cellular metabolism. Excessive ROS, however, cause oxidative stress, a state of imbalance between the production of ROS and the neutralization of free radicals by antioxidants, resulting in damage of cellular components including lipids, nucleic acids, metabolites, and proteins, which finally leads to the death of cells in plants. Thus, maintaining a physiological level of ROS is crucial for aerobic organisms, which relies on the combined operation of enzymatic and nonenzymatic antioxidants. In order to improve plants’ tolerance towards the harsh environment, it is vital to reinforce the comprehension of oxidative stress and antioxidant systems. In this review, recent findings on the metabolism of ROS as well as the antioxidative defense machinery are briefly updated. The latest findings on differential regulation of antioxidants at multiple levels under adverse environment are also discussed here.

Download Full-text

Differential response to water deficit stress and shade in two wheat (Triticum durum Desf.) cultivars: growth, water relations, osmolyte accumulation and photosynthetic pigments

Pakistan Journal of Botany ◽

10.30848/pjb2019-4(4) ◽

2019 ◽

Vol 51 (4) ◽

Cited By ~ 1

Author(s):

Fatma Gharbi ◽

Asma Guizani ◽

Lobna Zribi ◽

Hela Ben Ahmed ◽

Florent Mouillot

Keyword(s):

Water Deficit ◽

Water Relations ◽

Photosynthetic Pigments ◽

Triticum Durum ◽

Differential Response ◽

Water Deficit Stress ◽

Osmolyte Accumulation ◽

Triticum Durum Desf ◽

Response To Water

Download Full-text

Metabolic Profiling Analysis Reveals the Potential Contribution of Barley Sprouts against Oxidative Stress and Related Liver Cell Damage in Habitual Alcohol Drinkers

Antioxidants ◽

10.3390/antiox10030459 ◽

2021 ◽

Vol 10 (3) ◽

pp. 459

Author(s):

Hyerin Park ◽

Eunok Lee ◽

Yunsoo Kim ◽

Hye Yoon Jung ◽

Kwang-Min Kim ◽

...

Keyword(s):

Oxidative Stress ◽

Fatty Liver ◽

Molecular Mechanisms ◽

Learning Algorithm ◽

Controlled Trial ◽

Liver Fat ◽

Glutathione Metabolism ◽

Ros Generation ◽

Potential Contribution ◽

Glutamyl Transferase

Chronic excessive alcohol consumption is associated with multiple liver defects, such as steatosis and cirrhosis, mainly attributable to excessive reactive oxygen species (ROS) production. Barley sprouts (Hordeum vulgare L.) contain high levels of polyphenols that may serve as potential antioxidants. This study aimed to investigate whether barley sprouts extract powder (BSE) relieves alcohol-induced oxidative stress and related hepatic damages in habitual alcohol drinkers with fatty liver. In a 12-week randomized controlled trial with two arms (placebo or 480 mg/day BSE; n = 76), we measured clinical markers and metabolites at the baseline and endpoint to understand the complex molecular mechanisms. BSE supplementation reduced the magnitude of ROS generation and lipid peroxidation and improved the glutathione antioxidant system. Subsequent metabolomic analysis identified alterations in glutathione metabolism, amino acid metabolism, and fatty acid synthesis pathways, confirming the role of BSE in glutathione-related lipid metabolism. Finally, the unsupervised machine learning algorithm indicated that subjects with lower glutathione reductase at the baseline were responders for liver fat content, and those with higher fatigue and lipid oxidation were responders for γ-glutamyl transferase. These findings suggest that BSE administration may protect against hepatic injury by reducing oxidative stress and changing the metabolism in habitual alcohol drinkers with fatty liver.

Download Full-text

Protocatechuic Acid Protects Platelets from Apoptosis via Inhibiting Oxidative Stress-Mediated PI3K/Akt/GSK3β Signaling

Thrombosis and Haemostasis ◽

10.1055/s-0040-1722621 ◽

2021 ◽

Author(s):

Fuli Ya ◽

Kongyao Li ◽

Hong Chen ◽

Zezhong Tian ◽

Die Fan ◽

...

Keyword(s):

Oxidative Stress ◽

Caspase 3 ◽

Protocatechuic Acid ◽

Human Platelets ◽

Ros Generation ◽

Inhibitory Effects ◽

Platelet Apoptosis ◽

Phosphatidylserine Exposure ◽

Underlying Mechanisms

AbstractOxidative stress plays crucial roles in initiating platelet apoptosis that facilitates the progression of cardiovascular diseases (CVDs). Protocatechuic acid (PCA), a major metabolite of anthocyanin cyanidin-3-O-β-glucoside (Cy-3-g), exerts cardioprotective effects. However, underlying mechanisms responsible for such effects remain unclear. Here, we investigate the effect of PCA on platelet apoptosis and the underlying mechanisms in vitro. Isolated human platelets were treated with hydrogen peroxide (H2O2) to induce apoptosis with or without pretreatment with PCA. We found that PCA dose-dependently inhibited H2O2-induced platelet apoptosis by decreasing the dissipation of mitochondrial membrane potential, activation of caspase-9 and caspase-3, and decreasing phosphatidylserine exposure. Additionally, the distributions of Bax, Bcl-xL, and cytochrome c mediated by H2O2 in the mitochondria and the cytosol were also modulated by PCA treatment. Moreover, the inhibitory effects of PCA on platelet caspase-3 cleavage and phosphatidylserine exposure were mainly mediated by downregulating PI3K/Akt/GSK3β signaling. Furthermore, PCA dose-dependently decreased reactive oxygen species (ROS) generation and the intracellular Ca2+ concentration in platelets in response to H2O2. N-Acetyl cysteine (NAC), a ROS scavenger, markedly abolished H2O2-stimulated PI3K/Akt/GSK3β signaling, caspase-3 activation, and phosphatidylserine exposure. The combination of NAC and PCA did not show significant additive inhibitory effects on PI3K/Akt/GSK3β signaling and platelet apoptosis. Thus, our results suggest that PCA protects platelets from oxidative stress-induced apoptosis through downregulating ROS-mediated PI3K/Akt/GSK3β signaling, which may be responsible for cardioprotective roles of PCA in CVDs.

Download Full-text

Hydrogen Nano-Bubble Water Suppresses ROS Generation, Adipogenesis, and Interleukin-6 Secretion in Hydrogen-Peroxide- or PMA-Stimulated Adipocytes and Three-Dimensional Subcutaneous Adipose Equivalents

Cells ◽

10.3390/cells10030626 ◽

2021 ◽

Vol 10 (3) ◽

pp. 626

Author(s):

Li Xiao ◽

Nobuhiko Miwa

Keyword(s):

Oxidative Stress ◽

Hydrogen Peroxide ◽

Interleukin 6 ◽

Lipid Accumulation ◽

Metabolic Disorders ◽

Three Dimensional ◽

Human Keratinocytes ◽

Ros Generation ◽

Obese People ◽

Subcutaneous Adipose

Reactive oxygen species (ROS)-induced oxidative stress in adipose tissue is associated with inflammation and the development of obesity-related metabolic disorders. The aim of this study is to investigate the effects of hydrogen nano-bubble water (HW) on ROS generation, adipogenesis, and interleukin-6 (IL-6) secretion in hydrogen peroxide (H2O2) or phorbol 12-myristate 13-acetate (PMA)-stimulated OP9 adipocytes, and three-dimensional (3D) subcutaneous adipose equivalents. Nanoparticle tracking analysis showed that fresh HW contains 1.17 × 108/mL of nano-sized hydrogen bubbles. Even after 8 to 13 months of storage, approximately half of the bubbles still remained in the water. CellROX® staining showed that HW could diminish H2O2- or PMA-induced intracellular ROS generation in human keratinocytes HaCaT and OP9 cells. We discovered that PMA could markedly increase lipid accumulation to 180% and IL-6 secretion 2.7-fold in OP9 adipocytes. Similarly, H2O2 (5 µM) also significantly stimulated lipid accumulation in OP9 cells and the 3D adipose equivalents. HW treatment significantly repressed H2O2- or PMA-induced lipid accumulation and IL-6 secretion in OP9 adipocytes and the 3D adipose equivalents. In conclusion, HW showed a possibility of repressing oxidative stress, inflammatory response, and adipogenesis at cellular/tissue levels. It can be used for preventing the development of metabolic disorders amongst obese people.

Download Full-text

PERK mediates oxidative stress and adipogenesis in Graves’ orbitopathy pathogenesis

Journal of Molecular Endocrinology ◽

10.1530/jme-21-0057 ◽

2021 ◽

Author(s):

JaeSang Ko ◽

Ji-Young Kim ◽

Min Kyung Chae ◽

Eun Jig Lee ◽

Jin Sook Yoon

Keyword(s):

Oxidative Stress ◽

Hydrogen Peroxide ◽

Endoplasmic Reticulum ◽

Transcription Factor ◽

Er Stress ◽

Adipogenic Differentiation ◽

Ros Generation ◽

Mrna Levels ◽

Graves Orbitopathy ◽

Orbital Fibroblasts

We examined endoplasmic reticulum (ER) stress-related gene expression in orbital tissues from patients with Graves’ orbitopathy (GO) and the effects of silencing protein kinase RNA-like endoplasmic reticulum kinase (PERK) in primary orbital fibroblast cultures to demonstrate the therapeutic potential of PERK-modulating agents in GO management. The expression of ER stress related genes in orbital tissue harvested from individuals with or without GO was studied using real-time polymerase chain reaction. The role of PERK in GO pathogenesis was examined through small-interfering RNA (siRNA)-mediated silencing in cultured primary orbital fibroblasts. Intracellular reactive oxygen species (ROS) levels induced in response to cigarette smoke extract (CSE) or hydrogen peroxide were measured using 5-(and 6)-carboxy-20,70-dichlorodihydrofluorescein diacetate staining and flow cytometry. Cells were stained with Oil Red O, and adipogenesis-related transcription factor expression was evaluated through western blotting after adipogenic differentiation. PERK, activating transcription factor 4 (ATF4), and CCAAT-enhancer-binding protein (C/EBP)-homologous protein(CHOP)mRNA levels were significantly higher in GO orbital tissues than in non-GO orbital tissues. PERK silencing inhibited CSE- or hydrogen peroxide-induced ROS generation. After adipogenic differentiation, GO orbital fibroblasts revealed decreased lipid droplets and downregulation of C/EBPα, C/EBPβ, and peroxisome proliferator-activator gamma (PPARγ) in PERK siRNA-transfected cells. The orbital tissues of patients with GO were exposed to chronic ER stress and subsequently exhibited enhanced unfolded protein response (especially through the PERK pathway). PERK silencing reduced oxidative stress and adipogenesis in GO orbital fibroblasts in vitro. Our results imply that PERK-modulating agents can potentially be used to manage GO.

Download Full-text

Abstract 107: Apocynin Attenuates Isoproterenol-induced Myocardial Injury: Implications For Targeting Nadph Oxidase In Myocardial Fibrogenesis

Circulation Research ◽

10.1161/res.113.suppl_1.a107 ◽

2013 ◽

Vol 113 (suppl_1) ◽

Author(s):

Yu Chen ◽

Jingang Cui ◽

Qinbo Yang ◽

Chenglin Jia ◽

Minqi Xiong ◽

...

Keyword(s):

Oxidative Stress ◽

Nadph Oxidase ◽

Myocardial Fibrosis ◽

Myocardial Injury ◽

Oxidase Inhibitor ◽

Ros Generation ◽

Dependent Manner ◽

Expression Of Genes ◽

Therapeutic Development ◽

Myocardial Injuries

Myocardial fibrosis results from cardiac injuries caused by various pathophysiological mechanisms including myocardial infarction, leading to destruction of myocardial architecture and progressive cardiac dysfunction. Oxidative stress is likely involved in myocardial ischemic injury and the subsequent tissue remodeling mediated by myocardial fibrogenesis. Our current study aimed to evaluate the implication of NADPH oxidase in overproduction of reactive oxygen species and its contribution to the pathogenesis of myocardial fibrogenesis after ischemic injuries. The effects of Apocynin, a selective NADPH oxidase inhibitor, were evaluated in the mouse model of isoproterenol-induced myocardial injury by histopathological approaches and whole-genome gene expression profiling. The results demonstrated that Apocynin was able to inhibit the development of ISO-induced myocardial necrotic lesions and fibrogenesis in a dose-dependent manner. Moreover, the preventive effects of Apocynin on myocardial injuries were associated with suppressed expression of genes implicated in inflammation responses and extracellular matrix, which were remarkably upregulated by isoproterenol administration. In summary, o ur study provides proof-of-concept for the involvement of NADPH oxidase-mediated ROS generation in myocardial ischemic injuries and fibrogenesis, which will benefit the mechanism-based therapeutic development targeting NADPH oxidase and oxidative stress in treating myocardial fibrosis and related disorders.

Download Full-text

miR-187 modulates cardiomyocyte apoptosis and oxidative stress in myocardial infarction mice via negatively regulating DYRK2

10.22514/sv.2021.137 ◽

2021 ◽

Keyword(s):

Oxidative Stress ◽

Myocardial Infarction ◽

Protective Effect ◽

Myocardial Infarct ◽

Annexin V ◽

Cardiomyocyte Apoptosis ◽

Ros Generation ◽

Downstream Target

Myocardial infarction is a serious representation of cardiovescular disease, MicroRNAs play a role in modifying I/R injury and myocardial infarct remodeling. The present study therefore examined the potential role of miR-187 in cardiac I/R injury and its underlying mechanisms. miR-187 was inhibited or overexpressed in cardiomyocytes H/R models by pretreatment with miR-187 mimic or inhibitor to confirm the function of miR-187 in H/R. DYRK2 was inhibited or overexpressed in cardiomyocytes H/R models by pretreatment with DYRK2 inhibitor. A myocardium I/R mouse model was established. Circulating levels of miR-187 or DYRK2 was detected by quantitative realtime PCR and protein expression was detected by western blotting. The cell viability in all groups was determined by MTT assay and the apoptosis ratio was detected by flow cytometry after staining with Annexin V-FITC. The effect of miR-187 on cellular ROS generation was examined by DCFH-DA. The level of lipid peroxidation and SOD expression were determined by MDA and SOD assay. The findings indicated that miR-187 may be a possible regulator in the protective effect of H/R-induced cardiomyocyte apoptosis, cellular oxidative stress and leaded to DYRK2 suppression at a posttranscriptional level. Moreover, the improvement of miR-187 on H/R-induced cardiomyocyte injury contributed to the obstruction of DYRK2 expression. In addition, these results identified DYRK2 as the functional downstream target of miR-187 regulated myocardial infarction and oxidative stress.These present work provided the first insight into the function of miR-187 in successfully protect cardiomyocyte both in vivo and in vitro, and such a protective effect were mediated through the regulation of DYRK2 expression.

Download Full-text

Abstract MP30: Circulating Sars-cov-2 Spike Protein 1 Causes Microarteriolar Oxidative Stress, Endothelial Dysfunction And Enhanced Thromboxane And Endothelin Contractility That Are Prevented By Spironolactone.

Hypertension ◽

10.1161/hyp.78.suppl_1.mp30 ◽

2021 ◽

Vol 78 (Suppl_1) ◽

Author(s):

Dan Wang ◽

Christopher S Wilcox

Keyword(s):

Oxidative Stress ◽

Endothelial Cells ◽

Endothelial Dysfunction ◽

Fluorescence Microscopy ◽

Vascular Dysfunction ◽

Microvascular Complications ◽

Spike Protein ◽

Ros Generation ◽

Intravenous Injections ◽

Novel Model

Introduction and hypothesis: Following bodily entry, the SARS-CoV-2 virus undergoes pulmonary replication with release of circulating viral spike protein 1 (SP1) into the bloodstream. Uptake of SP1 by endothelial cells might provoke vascular dysfunction and thrombosis. We hypothesized that spironolactone could prevent microvascular complications from circulating SP1 in COVID-19. Methods: male C57Bl/6 mice received spironolactone (100 mg · kg -1 · d -1 PO x 3d) or vehicle and intravenous injections of recombinant full-length human SP1 (10 μg per mouse) or vehicle. They were euthanized after 3 days. Mesenteric resistant arterioles (n=4 per group) were dissected and mounted on isometric myographs. Acetylcholine-induced EDRF responses and L-NAME-inhibitable NO generation (DAF-FM fluorescence) were studied in pre-constricted vessels and contraction to endothelin 1 (ET1) or thromboxane (U-46, 619) and ET1-induced ROS (PEG-SOD inhibitable ethidium: dihydroethidium fluorescence) were studied by fluorescence microscopy in other vessels. Results: SP1 reduced acetylcholine-induced EDRF (17 ± 3 vs 27 ± 5 % mean ± sem; P < 0.05) and NO generation (0.21 ± 0.03 vs 0.36 ± 0.04, F 1 /F 0 ; P < 0.05) while increasing contraction to ET1 (10 -7 mol·l -1 : 124 ± 13 vs 89 ± 4 %; P < 0.05) and U-46, 619 (10 -6 mol·l -1 :114± 5 vs 87± 6 %; P < 0.05) and ET1-induced ROS generation(0.30± 0.08 vs 0.09± 0.03; P < 0.05). Spironolactone did not modify any of these responses in vessels from normal mice but prevented all the effects of SP1. Conclusion: these preliminary studies provide a novel model to study COVID-19 vasculopathy. They indicate that spironolactone can provide protection from microvascular oxidative stress, endothelial dysfunction and enhanced contractility and might thereby moderate COVID-19 complications.

Download Full-text