scholarly journals Utilizing Iron for Targeted Lipid Peroxidation as Anticancer Option of Integrative Biomedicine: A Short Review of Nanosystems Containing Iron

Antioxidants ◽  
2020 ◽  
Vol 9 (3) ◽  
pp. 191 ◽  
Author(s):  
Morana Jaganjac ◽  
Suzana Borovic Sunjic ◽  
Neven Zarkovic
Keyword(s):  
Oxidative Stress ◽  
Lipid Peroxidation ◽  
Defense Mechanism ◽  
Redox Homeostasis ◽  
Life Sciences ◽  
Short Review ◽  
Oxidative Capacity ◽  
Chain Reactions ◽  
Fundamental Process ◽  
Magnetic Dynamic

Traditional concepts of life sciences consider oxidative stress as a fundamental process of aging and various diseases including cancer, whereas traditional medicine recommends dietary intake of iron to support physiological functions of the organism. However, due to its strong pro-oxidative capacity, if not controlled well, iron can trigger harmful oxidative stress manifested eventually by toxic chain reactions of lipid peroxidation. Such effects of iron are considered to be major disadvantages of uncontrolled iron usage, although ferroptosis seems to be an important defense mechanism attenuating cancer development. Therefore, a variety of iron-containing nanoparticles were developed for experimental radio-, chemo-, and photodynamic as well as magnetic dynamic nanosystems that alter redox homeostasis in cancer cells. Moreover, studies carried over recent decades have revealed that even the end products of lipid peroxidation, represented by 4-hydroxynonenal (4-HNE), could have desirable effects even acting as kinds of selective anticancer substances produced by non-malignant cells for defense again invading cancer. Therefore, advanced nanotechnologies should be developed for using iron to trigger targeted lipid peroxidation as an anticancer option of integrative biomedicine.

scholarly journals Staphylococcus aureususes the bacilliredoxin (BrxAB)/ bacillithiol disulfide reductase (YpdA) redox pathway to defend against oxidative stress under infections

2019 ◽  
Author(s):  
Nico Linzner ◽  
Vu Van Loi ◽  
Verena Nadin Fritsch ◽  
Quach Ngoc Tung ◽  
Saskia Stenzel ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Defense Mechanism ◽  
Redox Homeostasis ◽  
Stress Monitoring ◽  
Macrophage Infection ◽  
Disulfide Reductase ◽  
Mixed Disulfides

ABSTRACTStaphylococcus aureusis a major human pathogen and has to cope with reactive oxygen and chlorine species (ROS, RCS) during infections. The low molecular weight thiol bacillithiol (BSH) is an important defense mechanism ofS. aureusfor detoxification of ROS and HOCl stress to maintain the reduced state of the cytoplasm. Under HOCl stress, BSH forms mixed disulfides with proteins, termed asS-bacillithiolations, which are reduced by bacilliredoxins (BrxA and BrxB). The NADPH-dependent flavin disulfide reductase YpdA is phylogenetically associated with the BSH synthesis and BrxA/B enzymes and was proposed to function as BSSB reductase. Here, we investigated the role of the bacilliredoxin BrxAB/BSH/YpdA pathway inS. aureusCOL under oxidative stress and macrophage infection conditionsin vivoand in biochemical assaysin vitro. Using HPLC thiol metabolomics, a strongly enhanced BSSB level and a decreased BSH/BSSB ratio were measured in theS. aureusCOLypdAdeletion mutant under control and NaOCl stress. Monitoring the BSH redox potential (EBSH) using the Brx-roGFP2 biosensor revealed that YpdA is required for regeneration of the reducedEBSHupon recovery from oxidative stress. In addition, theypdAmutant was impaired in H2O2detoxification as measured with the novel H2O2-specific Tpx-roGFP2 biosensor. Phenotype analyses further showed that BrxA and YpdA are required for survival under NaOCl and H2O2stressin vitroand inside murine J-774A.1 macrophages in infection assaysin vivo. Finally, NADPH-coupled electron transfer assays provide evidence for the function of YpdA in BSSB reduction, which depends on the conserved Cys14 residue. YpdA acts together with BrxA and BSH in de-bacillithiolation ofS-bacilithiolated GapDH. In conclusion, our results point to a major role of the BrxA/BSH/YpdA pathway in BSH redox homeostasis inS. aureusduring recovery from oxidative stress and under infections.

Is atherosclerosis a mitochondrial disorder?

VASA ◽  
2007 ◽  
Vol 36 (4) ◽  
pp. 229-240 ◽  
Author(s):  
Finsterer
Keyword(s):  
Oxidative Stress ◽  
Risk Factors ◽  
Lipid Peroxidation ◽  
Redox Homeostasis ◽  
Mitochondrial Disorder ◽  
Vascular Wall ◽  
Nitrogen Species ◽  
Key Factors ◽  
Caspase Cascade ◽  
And Function

There is increasing evidence that damage to the vascular environment from oxidative stress plays a major role in the pathogenesis of atherosclerosis in addition to classical risk factors, such as age, arterial hypertension, diabetes, dyslipidemia, smoking, vascular wall inflammation, or genetic predisposition. Oxidative stress results from the endogenous or exogenous generation of reactive oxidative or nitrogen species, generated by the respiratory chain or enzymatic sources. Oxidative stress results in lipid peroxidation, damage of mitochondrial components including mitochondrial DNA, mitochondrial dysfunction, damage of endothelial cells, vascular smooth muscle cells, and erythrocytes, and lastly apoptosis via either the receptor-mediated pathway or the mitochondria-mediated pathway and activation of the caspase cascade. Though re-balancing of the redox homeostasis by various agents is clinically hardly effective, various trials with experimental agents are promising in this respect. Overall, atherosclerosis appears to be the endpoint of various different pathogenetic mechanisms, of which oxidative stress and disturbed mitochondrial metabolism and function are key factors.

The co-expression of 4-hydroxynonenal and prominin-1 in glioblastomas

2011 ◽  
Vol 2 (2) ◽  
Author(s):  
Danijela Kolenc ◽  
Antonia Jakovčević ◽  
Marija Macan ◽  
Kamelija Žarković
Keyword(s):  
Oxidative Stress ◽  
Lipid Peroxidation ◽  
Bone Marrow ◽  
Endothelial Cells ◽  
Important Implication ◽  
Oxidative Capacity ◽  
Surface Marker ◽  
Astrocytic Tumors ◽  
Main Hypothesis ◽  
Excess Production

AbstractOxidative stress (OS) is the condition that occurs when the anti-oxidative capacity of tissues and cells is overcome. The oxidative damage of cells is caused by free radicals which are products of OS. Lipid peroxidation is an autocatalitic process caused by OS which damages lipids and causes production of highly reactive species such as 4-hyroxynonenal (HNE). Recent findings have shown an increase in HNE-immunopositivity when compared to grade of astrocytic tumors. The cancer stem cell hypothesis suggests that not all cells in the tumor have the same ability to proliferate and maintain the growth of the tumor. Only a relatively small fraction of cells in the tumor, termed cancer stem cells, posses the ability to proliferate and self-renew extensively and expresses the surface marker CD133 (prominin-1). CNS tissue damage via trauma, viruses and ishaemia, increases the amount of OS production, which damages endothelial cells and consequently results in excess production of bone marrow-derived endothelial progenitor cells (EPCs). EPCs are immunoreactive for CD133 and CD34 and are thus important in the process of angiogenesis. Results of our study confirmed the main hypothesis, i.e.the proportional expression and distribution of CD133 and HNE in tumor cells, mesenchymal stroma, blood vessels and in the areas of necrosis, probably due to permanent OS in tumors, whose products continue to damage the endothelial cells and cause an excess production of EPCs. Identification of coexpression HNE and CD133 in GBM has important implication for the understanding of propagation of tumors into higher grade.

scholarly journals Antioxidative defense mechanism of the ruderal Verbascum olympicum Boiss. against copper (Cu)-induced stress

2016 ◽  
Vol 11 (1) ◽  
pp. 10-20 ◽  
Author(s):  
Ayşegül Uğar Akpınar ◽  
Hülya Arslan ◽  
Gürcan Güleryüz ◽  
Serap Kırmızı
Keyword(s):  
Oxidative Stress ◽  
Lipid Peroxidation ◽  
Defense Mechanism ◽  
Growth Parameters ◽  
Antioxidative Defense ◽  
Membrane Injury ◽  
Induced Stress ◽  
Hoagland Nutrient Solution ◽  
Hydroponic Conditions

AbstractThe endemic Verbascum olympicum has characteristics that allows it to live in degraded areas of Uludağ Mountain, Turkey and therefore known as a ruderal species. In this study, V. olympicum seeds collected from Uludağ Mountain were grown in the Hoagland nutrient solution, under hydroponic conditions. The activity of antioxidative enzymes (superoxide dismutase, SOD; catalase, CAT; ascorbate peroxidase, APX) were examined to demonstrate the role of antioxidative mechanism in the seedlings exposed to different Cu concentrations (0, 50, 250, 500 μM) for seven days. Also, certain growth parameters (such as the water content, biomass production, soluble protein), the level of lipid peroxidation, cell membrane injury and permeability were investigated. As a result, some toxic effects are observed following the application of 500 μM Cu, after the seedlings growing in 50 and 250 mM Cu concentrations showed high resistance and survived in hydroponic conditions. Our findings provide information about the resistance of V. Olympicum seedlings to oxidative stress caused by excessive Cu concentrations.

scholarly journals Effect of Exogenous Treatment with Nitric Oxide (NO) on Redox Homeostasis in Barley Seedlings (Hordeum vulgare L.) Under Copper Stress

2022 ◽  
Author(s):  
Marouane Ben Massoud ◽  
Oussama Kharbech ◽  
Yathreb Mahjoubi ◽  
Abdelilah Chaoui ◽  
Astrid Wingler
Keyword(s):  
Oxidative Stress ◽  
Nitric Oxide ◽  
Lipid Peroxidation ◽  
Hordeum Vulgare ◽  
Antioxidant Enzyme ◽  
Enzyme Activities ◽  
Redox Homeostasis ◽  
Copper Stress ◽  
Antioxidant Enzyme Activities ◽  
Cu Toxicity

AbstractThe protective mechanism of nitric oxide (NO) in regulating tolerance to Cu-induced toxicity in shoots of barley (Hordeum vulgare L.) was studied. The experiment consisted of four treatments based on additions to basal nutrient solutions (BNS): control (CTR), Cu (200 µM), SNP (500 µM), and Cu (200 µM) + SNP (500 µM) over a period of 10 days. Treatment with Cu significantly reduced seedling growth and photosynthetic efficiency concomitant with an increase in reactive oxygen species contents, lipid peroxidation markers, and antioxidant enzyme activities, indicating that Cu induced oxidative stress. Furthermore, growth inhibition of Cu-treated plants was associated with a reduction in photosynthetic pigments and maximum photosystem II efficiency as well as a strong decrease in levels of glutathione (GSH) and ascorbate (AsA). Addition of a nitric oxide (NO) donor, sodium nitroprusside (SNP), to the growth medium alleviated Cu toxicity by decreasing Cu uptake and enhancing antioxidant capacity, as indicated by increased contents of GSH and AsA. The application of SNP decreased oxidative stress and lipid peroxidation by suppressing lipoxygenase activity and enhancing some antioxidant enzyme activities. The results obtained indicate the potential of exogenously applied SNP in the management of metal toxicity. Hence, NO generating compounds have potential agronomical applications when cultivating in contaminated areas. Our findings indicate that NO can alleviate Cu toxicity by affecting the antioxidant defense system and maintaining the glutathione-ascorbate cycle status, suggesting that SNP treatment protects proteins against oxidation by regulating the cellular redox homeostasis.

scholarly journals Chronic Hyperinsulinaemic Hypoglycaemia in Rats Is Accompanied by Increased Body Weight, Hyperleptinaemia, and Decreased Neuronal Glucose Transporter Levels in the Brain

2017 ◽  
Vol 2017 ◽  
pp. 1-14 ◽  
Author(s):  
Vivi F. H. Jensen ◽  
Anne-Marie Mølck ◽  
Melissa Chapman ◽  
Lene Alifrangis ◽  
Lene Andersen ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Lipid Peroxidation ◽  
Body Weight ◽  
Food Consumption ◽  
Glucose Transporter ◽  
Redox Homeostasis ◽  
Hyperinsulinaemic Hypoglycaemia ◽  
Lipid Peroxidation Products ◽  
Glucose Levels ◽  
The Brain

The brain is vulnerable to hypoglycaemia due to a continuous need of energy substrates to meet its high metabolic demands. Studies have shown that severe acute insulin-induced hypoglycaemia results in oxidative stress in the rat brain, when neuroglycopenia cannot be evaded despite increased levels of cerebral glucose transporters. Compensatory measures in the brain during chronic insulin-induced hypoglycaemia are less well understood. The present study investigated how the brain of nondiabetic rats copes with chronic insulin-induced hypoglycaemia for up to eight weeks. Brain level of different substrate transporters and redox homeostasis was evaluated. Hyperinsulinaemia for 8 weeks consistently lowered blood glucose levels by 30–50% (4–6 mM versus 7–9 mM in controls). The animals had increased food consumption, body weights, and hyperleptinaemia. During infusion, protein levels of the brain neuronal glucose transporter were decreased, whereas levels of lipid peroxidation products were unchanged. Discontinued infusion was followed by transient systemic hyperglycaemia and decreased food consumption and body weight. After 4 weeks, plasma levels of lipid peroxidation products were increased, possibly as a consequence of hyperglycaemia-induced oxidative stress. The present data suggests that chronic moderate hyperinsulinaemic hypoglycaemia causes increased body weight and hyperleptinaemia. This is accompanied by decreased neuronal glucose transporter levels, which may be leptin-induced.

Correlation of testicular toxicity and oxidative stress induced by chlorpyrifos in rats

2011 ◽  
Vol 30 (10) ◽  
pp. 1529-1539 ◽  
Author(s):  
Tapas Kumar Mandal ◽  
Niladri Sekhar Das
Keyword(s):  
Oxidative Stress ◽  
Lipid Peroxidation ◽  
Body Weight ◽  
Antioxidant Enzymes ◽  
Defense Mechanism ◽  
Seminiferous Tubules ◽  
Converting Enzyme ◽  
Diene Conjugates ◽  
Stress Changes ◽  
Higher Doses

Effect of chlorpyrifos pesticide on testicular oxidative damage was studied in Sprague-Dawley rats at varying doses. At lower doses (5 and 10 mg/kg body weight/30 days), reduction in plasma levels of testosterone and follicular stimulating hormone (FSH) and luteinizing hormone (LH) along with significant shrinkage of seminiferous tubules and drastic changes in germ cells were seen. But these adverse changes of testes were restored with the revival of serum testosterone and FSH and LH at higher doses (20 and 30 mg/kg body weight/30 days). Similarly, levels of testicular lipid peroxidation and diene conjugates were elevated whereas activities of antioxidant enzymes (superoxide dismutase, catalase and glutathione peroxidase), steroidogenic (Δ5, 3β-HSD and Δ5, 17β-HSD) enzymes and angiotensinogen-converting enzyme and glutathione content including lipid–protein content of testes were decreased at low doses. But at higher doses, reductions in level of lipid peroxidation (as revealed by malondialdehyde [MDA] value) and conjugated dienes were found and on the contrary, revivals of testicular antiperoxidative/antioxidant enzymes defense systems, angiotensinogen-converting enzyme (ACE), steroidogenic enzymes, lipid–protein and antioxidant glutathione content were observed. Therefore, the present study indicated from the results that chlorpyrifos had a dual effect at both doses on oxidative stress changes, but at higher doses, the cells were triggering its natural defense mechanism to combat the insult of lower doses of chlorpyrifos and became operative possibly through corrective measure of antioxidant enzymes defense system and pituitary gonadotropins hormones feedback mechanisms on testes.

scholarly journals Reactive Oxygen Species, Lipid Peroxidation and Antioxidative Defense Mechanism

2013 ◽  
Vol 41 (1) ◽  
pp. 44 ◽  
Author(s):  
Hossam S. EL-BELTAGI ◽  
Heba I. MOHAMED
Keyword(s):  
Oxidative Stress ◽  
Lipid Peroxidation ◽  
Carbonyl Compounds ◽  
Defense Mechanism ◽  
Lipid Peroxides ◽  
Cellular Injury ◽  
Oxygen Species ◽  
Antioxidative Defense ◽  
Inhibit Lipid Peroxidation ◽  
Reactive Carbonyl Compounds

Lipid peroxidation can be defined as the oxidative deterioration of lipids containing any number of carbon-carbon double bonds. Lipid peroxidation is a well-established mechanism of cellular injury in both plants and animals, and is used as an indicator of oxidative stress in cells and tissues. Lipid peroxides are unstable and decompose to form a complex series of compounds including reactive carbonyl compounds. The oxidation of linoleates and cholesterol is discussed in some detail. Analytical methods for studying lipid peroxidation were mentioned. Various kinds of antioxidants with different functions inhibit lipid peroxidation and the deleterious effects caused by the lipid peroxidation products.

Changes in lipid peroxidation during pregnancy and after delivery in rats: effect of pinealectomy

Reproduction ◽  
2000 ◽  
pp. 143-149 ◽  
Author(s):  
RM Sainz ◽  
RJ Reiter ◽  
JC Mayo ◽  
J Cabrera ◽  
DX Tan ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Lipid Peroxidation ◽  
Oxidative Damage ◽  
Energy Demand ◽  
Physiological State ◽  
High Energy ◽  
Free Radical Scavengers ◽  
Radical Scavengers ◽  
Oxygen Requirement ◽  
Pregnant Rats

Pregnancy is a physiological state accompanied by a high energy demand of many bodily functions and an increased oxygen requirement. Because of the increased intake and utilization of oxygen, increased levels of oxidative stress would be expected. In the present study, the degree of lipid peroxidation was examined in different tissues from non-pregnant and pregnant rats after the delivery of their young. Melatonin and other indole metabolites are known to be direct free radical scavengers and indirect antioxidants. Thus the effect of pinealectomy at 1 month before pregnancy on the accumulation of lipid damage was investigated in non-pregnant and pregnant rats after the delivery of their young. Malonaldehyde and 4-hydroxyalkenal concentrations were measured in the lung, uterus, liver, brain, kidney, thymus and spleen from intact and pinealectomized pregnant rats soon after birth of their young and at 14 and 21 days after delivery. The same parameters were also evaluated in intact and pinealectomized non-pregnant rats. Shortly after delivery, lipid oxidative damage was increased in lung, uterus, brain, kidney and thymus of the mothers. No differences were detected in liver and spleen. Pinealectomy enhanced this effect in the uterus and lung. It is concluded that during pregnancy high levels of oxidative stress induce an increase in oxidative damage to lipids, which in some cases is inhibited by the antioxidative actions of pineal indoles.

Resistance of erythrocytes from Brown trout (Salmo trutta m. trutta L.) affected by ulcerative dermal necrosis syndrome

2011 ◽  
Vol 14 (3) ◽  
pp. 443-448 ◽  
Author(s):  
N. Kurhalyuk ◽  
H. Tkachenko ◽  
K. Pałczyńska
Keyword(s):  
Oxidative Stress ◽  
Lipid Peroxidation ◽  
Brown Trout ◽  
Salmo Trutta ◽  
Thiobarbituric Acid ◽  
Control Group ◽  
Thiobarbituric Acid Reactive Substance ◽  
Tbars Level ◽  
Reactive Substance ◽  
Brown Trout Salmo Trutta

Resistance of erythrocytes from Brown trout (Salmo trutta m. trutta L.) affected by ulcerative dermal necrosis syndrome In the present work we evaluated the effect of ulcerative dermal necrosis (UDN) syndrome on resistance of erythrocytes to haemolytic agents and lipid peroxidation level in the blood from brown trout (Salmo trutta m. trutta L.). Results showed that lipid peroxidation increased in erythrocytes, as evidenced by high thiobarbituric acid reactive substance (TBARS) levels. Compared to control group, the resistance of erythrocytes to haemolytic agents was significantly lower in UDN-positive fish. Besides, UDN increased the percent of hemolysated erythrocytes subjected to the hydrochloric acid, urea and hydrogen peroxide. Results showed that UDN led to an oxidative stress in erythrocytes able to induce enhanced lipid peroxidation level, as suggested by TBARS level and decrease of erythrocytes resistance to haemolytic agents.

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