scholarly journals Malondialdehyde as a Prognostic Marker in Patients with Ovarian Adenocarcinoma

2019 ◽  
Vol 70 (7) ◽  
pp. 2561-2565
Author(s):  
Oana Trifanescu ◽  
Maria Iuliana Gruia ◽  
Laurentia Gales ◽  
Raluca Trifanescu ◽  
Alina Mihaela Pascu ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Lipid Peroxidation ◽  
Genetic Instability ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Invasion And Metastasis ◽  
Prognostic Role ◽  
Ovarian Adenocarcinoma

Oxidative stress is defined as the imbalance between reactive oxygen species and cellular antioxidative mechanisms. Reactive oxygen species are involved in the development and progression of many cancers and has been showed to activate pro-tumorigenic signalling, increase tumour cell survival, proliferation, invasion and metastasis, DNA damage and genetic instability. These are highly reactive and attack various classes of essentials biomolecules such as proteins, DNA and most important lipids. Malondialdehyde is the best investigated product of lipid peroxidation. The aim of this study was to evaluate the prognostic role of malondialdehyde in patients with ovarian adenocarcinoma and in an experimental model.

scholarly journals The role of oxidative/nitrosative stress in pathogenesis of paracetamol-induced toxic hepatitis

2010 ◽  
Vol 63 (11-12) ◽  
pp. 827-832 ◽  
Author(s):  
Tatjana Radosavljevic ◽  
Dusan Mladenovic ◽  
Danijela Vucevic ◽  
Rada Jesic-Vukicevic
Keyword(s):  
Oxidative Stress ◽  
Nitric Oxide ◽  
Reactive Oxygen Species ◽  
Liver Injury ◽  
Kupffer Cells ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Severe Liver ◽  
Hepatocellular Necrosis

Introduction. Paracetamol is an effective analgesic/antipyretic drug when used at therapeutic doses. However, the overdose of paracetamol can cause severe liver injury and liver necrosis. The mechanism of paracetamol-induced liver injury is still not completely understood. Reactive metabolite formation, depletion of glutathione and alkylation of proteins are the triggers of inhibition of mitochondrial respiration, adenosine triphosphate depletion and mitochondrial oxidant stress leading to hepatocellular necrosis. Role of oxidative stress in paracetamol-induced liver injury. The importance of oxidative stress in paracetamol hepatotoxicity is controversial. Paracetamol induced liver injury cause the formation of reactive oxygen species. The potent sources of reactive oxygen are mitochondria, neutrophils, Kupffer cells and the enzyme xatnine oxidase. Free radicals lead to lipid peroxidation, enzymatic inactivation and protein oxidation. Role of mitochondria in paracetamol-induced oxidative stress. The production of mitochondrial reactive oxygen species is increased, and the glutathione content is decreased in paracetamol overdose. Oxidative stress in mitochondria leads to mito?chondrial dysfunction with adenosine triphosphate depletion, increase mitochondrial permeability transition, deoxyribonu?cleic acid fragmentation which contribute to the development of hepatocellular necrosis in the liver after paracetamol overdose. Role of Kupffer cells in paracetamol-induced liver injury. Paracetamol activates Kupffer cells, which then release numerous cytokines and signalling molecules, including nitric oxide and superoxide. Kupffer cells are important in peroxynitrite formation. On the other hand, the activated Kupffer cells release anti-inflammatory cytokines. Role of neutrophils in paracetamol-induced liver injury. Paracetamol-induced liver injury leads to the accumulation of neutrophils, which release lysosomal enzymes and generate superoxide anion radicals through the enzyme nicotinamide adenine dinucleotide phosphate oxidase. Hydrogen peroxide, which is influenced by the neutrophil-derived enzyme myeloperoxidase, generates hypochlorus acid as a potent oxidant. Role of peroxynitrite in paracetamol-induced oxidative stress. Superoxide can react with nitric oxide to form peroxynitrite, as a potent oxidant. Nitrotyrosine is formed by the reaction of tyrosine with peroxynitrite in paracetamol hepatotoxicity. Conclusion. Overdose of paracetamol may produce severe liver injury with hepatocellular necrosis. The most important mechanisms of cell injury are metabolic activation of paracetamol, glutathione depletion, alkylation of proteins, especially mitochondrial proteins, and formation of reactive oxygen/nitrogen species.

scholarly journals Ginkgo biloba extract (EGb 761) attenuates oxidative stress induction in erythrocytes of sickle cell disease patients

2012 ◽  
Vol 48 (4) ◽  
pp. 659-665 ◽  
Author(s):  
Aline Emmer Ferreira Furman ◽  
Railson Henneberg ◽  
Priscila Bacarin Hermann ◽  
Maria Suely Soares Leonart ◽  
Aguinaldo José do Nascimento
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Lipid Peroxidation ◽  
Sickle Cell ◽  
Reduced Glutathione ◽  
Reactive Oxygen ◽  
Intracellular Reactive Oxygen Species ◽  
Oxygen Species ◽  
Egb 761 ◽  
Cell Disease

Sickle cell disease promotes hemolytic anemia and occlusion of small blood vessels due to the presence of high concentrations of hemoglobin S, resulting in increased production of reactive oxygen species and decreased antioxidant defense capacity. The aim of this study was to evaluate the protective action of a standardized extract of Ginkgo biloba (EGb 761), selected due to its high content of flavonoids and terpenoids, in erythrocytes of patients with sickle cell anemia (HbSS, SS erythrocytes) subjected to oxidative stress using tert-butylhydroperoxide or 2,2-azobis-(amidinepropane)-dihydrochloride, in vitro. Hemolysis indexes, reduced glutathione, methemoglobin concentrations, lipid peroxidation, and intracellular reactive oxygen species were determined. SS erythrocytes displayed increased rates of oxidation of hemoglobin and membrane lipid peroxidation compared to normal erythrocytes (HbAA, AA erythrocytes), and the concentration of EGb 761 necessary to achieve the same antioxidant effect in SS erythrocytes was at least two times higher than in normal ones, inhibiting the formation of intracellular reactive oxygen species (IC50 of 13.6 µg/mL), partially preventing lipid peroxidation (IC50 of 242.5 µg/mL) and preventing hemolysis (IC50 of 10.5 µg/mL). Thus, EGb 761 has a beneficial effect on the oxidative status of SS erythrocytes. Moreover, EGb 761 failed to prevent oxidation of hemoglobin and reduced glutathione at the concentrations examined.

scholarly journals Antioxidant effect of Mn2+ on capacitation and acrosome reaction of fresh and chilled cattle bull semen

2012 ◽  
Vol 1 (1) ◽  
pp. 18
Author(s):  
Amrit Kaur Bansal ◽  
Ranjna Sundhey Cheema ◽  
Vinod Kumar Gandotra
Keyword(s):  
Reactive Oxygen Species ◽  
Lipid Peroxidation ◽  
Acrosome Reaction ◽  
Reactive Oxygen ◽  
Antioxidant Effect ◽  
Oxygen Species ◽  
Sperm Capacitation ◽  
Bull Semen

The aim of this paper was to investigate the antioxidant effect of Mn2+ (200 mM) on the sperm capacitation and acrosome reaction of fresh and chilled cattle bull semen. It has been found that Mn2+ supplementation improves (P≤0.05) the motility at 0, 2, 4 and 6 h of incubation. MDA (malondialdehyde), end product of lipid peroxidation, decreases significantly (P≤0.05) with the supplementation of manganese at 0- and 6-hr of incubation both in fresh and chilled semen. Manganese also increases acrosome reaction significantly (P≤0.05) both in fresh and chilled semen at 0, 4 and 6 h of incubation. Therefore, our findings suggest the role of Mn2+supplementation in improving the quality of cattle bull semen by its scavenging property<em> i.e.</em> reduction in the production of reactive oxygen species during its storage at 4°C or incubation at 37°C for capacitation.

scholarly journals NADPH Oxidase as a Therapeutic Target for Oxalate Induced Injury in Kidneys

2013 ◽  
Vol 2013 ◽  
pp. 1-18 ◽  
Author(s):  
Sunil Joshi ◽  
Ammon B. Peck ◽  
Saeed R. Khan
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Nadph Oxidase ◽  
Tissue Injury ◽  
Nicotinamide Adenine Dinucleotide Phosphate ◽  
Reactive Oxygen ◽  
Renal Tissue ◽  
Oxygen Species ◽  
Gene Expressions

A major role of the nicotinamide adenine dinucleotide phosphate (NADPH) oxidase family of enzymes is to catalyze the production of superoxides and other reactive oxygen species (ROS). These ROS, in turn, play a key role as messengers in cell signal transduction and cell cycling, but when they are produced in excess they can lead to oxidative stress (OS). Oxidative stress in the kidneys is now considered a major cause of renal injury and inflammation, giving rise to a variety of pathological disorders. In this review, we discuss the putative role of oxalate in producing oxidative stress via the production of reactive oxygen species by isoforms of NADPH oxidases expressed in different cellular locations of the kidneys. Most renal cells produce ROS, and recent data indicate a direct correlation between upregulated gene expressions of NADPH oxidase, ROS, and inflammation. Renal tissue expression of multiple NADPH oxidase isoforms most likely will impact the future use of different antioxidants and NADPH oxidase inhibitors to minimize OS and renal tissue injury in hyperoxaluria-induced kidney stone disease.

Flavonoids, the Family of Plant-derived Antioxidants making inroads into Novel Therapeutic Design against IR-induced Oxidative Stress in Parkinson’s Disease

2021 ◽  
Vol 19 ◽  
Author(s):  
Tapan Behl ◽  
Gagandeep Kaur ◽  
Aayush Sehgal ◽  
Gokhan Zengin ◽  
Sukhbir Singh ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Ionizing Radiation ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Radiation Induced ◽  
Novel Therapeutic

Background: Ionizing radiation from telluric sources is unceasingly an unprotected pitfall to humans. Thus, the foremost contributors to human exposure are global and medical radiations. Various pieces of evidences assembled during preceding years reveal the pertinent role of ionizing radiation-induced oxidative stress in the progression of neurodegenerative insults such as Parkinson’s disease, which have been contributing to increased proliferation and generation of reactive oxygen species. Objective: This review delineates the role of ionizing radiation-induced oxidative stress in Parkinson’s disease and proposes novel therapeutic interventions of flavonoid family offering effective management and slowing down the progression of Parkinson’s disease. Method: Published papers were searched via MEDLINE, PubMed, etc. published to date for in-depth database collection. Results: The potential of oxidative damage may harm the non-targeted cells. It can also modulate the functions of central nervous system, such as protein misfolding, mitochondria dysfunction, increased levels of oxidized lipids, and dopaminergic cell death, which accelerates the progression of Parkinson’s disease at the molecular, cellular, or tissue levels. In Parkinson’s disease, reactive oxygen species exacerbate the production of nitric oxides and superoxides by activated microglia, rendering death of dopaminergic neuronal cell through different mechanisms. Conclusion: Rising interest has extensively engrossed on the clinical trial designs based on the plant derived family of antioxidants. They are known to exert multifarious impact either way in neuroprotection via directly suppressing ionizing radiation-induced oxidative stress and reactive oxygen species production or indirectly increasing the dopamine levels and activating the glial cells.

Reactive oxygen species in patients with ovarian adenocarcinoma treated with platinum based chemotherapy.

2017 ◽  
Vol 35 (15_suppl) ◽  
pp. e17047-e17047
Author(s):  
Anghel Rodica Maricela ◽  
Laurentia Gales ◽  
Maria Iuliana Gruia ◽  
Raluca Alexandra Trifanescu ◽  
Fabiana Curea ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Lipid Peroxidation ◽  
Reactive Oxygen ◽  
Mean Value ◽  
Oxygen Species ◽  
Ovarian Adenocarcinoma ◽  
Stage Iiic ◽  
Normal Value ◽  
Platinum Based Chemotherapy ◽  
Platinum Salt

e17047 Background: Ovarian adenocarcinoma (OA) is the most lethal of gynecologic tumors because women generally present with advanced stage disease. Platinum-based chemotherapy plays a pivotal role in OA treatment. The aim of the study was to assess the role of oxygen species in patients with OA and the effects of platinum based chemotherapy on blood redox status. Methods: Twenty three patients with advanced stage IIIC or IV OA who underwent platinum salts chemotherapy were included. Blood sample were collected before treatment, at 21 days (second cycle of chemotherapy) and at 42 days (3rd cycle) and at 63 day (4th cycle) with a platinum salt (cisplatin or carboplatin). Biochemical determination of oxidative stress was made by mesuring lipid peroxidation index (LPI), the enzymatic activity of ceruloplasmin and the thiol albumin groups. Results: Median age at diagnosis was 52 years, and 47.8% of patients presented with stage IIIC and 52.2% with stage IV. Nine patients received for the first time platinum based chemotherapy and 14 received multiple lines of chemotherapy. Response rate after 4 cycles were partial in 30%, stable disease in 57%, and progression disease in 13%. Mean value (± SD) of lipid peroxides was 6.81±1.μmol/100 ml (normal value 0-4), and of ceruloplasmin 156 ± 66 UI (normal value 80-120) which showed an increase of the final products of lipid peroxidation. Thiol mean value was 296±124 μmol/l (normal value 370- 450). The evolution of these reactive oxygen species were monitored during chemotherapy cycles. Decrease of the lipid peroxidation after 1st cycle was noticed, (7, 6.89, 5.87, 6.61), because platinum salt can bind peroxyde and this can be considered a marker of effectiveness of treatment.The thiol levels increased from one cycle to other (233, 311, 384, 393) showing that the cell is trying to contracarete the oxidative stress. Conclusions: Tumors produces reactive oxygen species in excess in patients with advanced OA. Platinum based chemotherapy in patients with OA induces radical formation and the dynamic of these markers may be used to monitor response to treatment.

Magnesium deficiency augments myocardial response to reactive oxygen species

2006 ◽  
Vol 84 (6) ◽  
pp. 617-624 ◽  
Author(s):  
L. Manju ◽  
R. Renuka Nair
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Lipid Peroxidation ◽  
Tissue Injury ◽  
Ischemia Reperfusion ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Inotropic Response ◽  
Mg Deficiency ◽  
Negative Inotropic Response

Magnesium (Mg) deficiency and oxidative stress are independently implicated in the etiopathogenesis of various cardiovascular disorders. This study was undertaken to examine the hypothesis that Mg deficiency augments the myocardial response to oxidative stress. Electrically stimulated rat papillary muscle was used for recording the contractile variation. Biochemical variables of energy metabolism (adenosine triphosphate (ATP) and creatine phosphate) and markers of tissue injury (lactate dehydrogenase (LDH) release and lipidperoxidation), which can affect myocardial contractility, were assayed in Langendorff-perfused rat hearts. Hydrogen peroxide (100 µmol/L) was used as the source of reactive oxygen species. The negative inotropic response to H2O2 was significantly higher in Mg deficiency (0.48 mmol Mg/L) than in Mg sufficiency (1.2 mmol Mg/L). Low Mg levels did not affect ATP levels or tissue lipid peroxidation. However, H2O2 induced a decrease in ATP; enhanced lipid peroxidation and the release of LDH were augmented by Mg deficiency. Increased lipid peroxidation associated with a decrease in available energy might be responsible for the augmentation of the negative inotropic response to H2O2 in Mg deficiency. The observations from this study validate the hypothesis that myocardial response to oxidative stress is augmented by Mg deficiency. This observation has significance in ischemia–reperfusion injury, where Mg deficiency can have an additive effect on the debilitating consequences.

Free radicals, lipid peroxidation and sperm function

1995 ◽  
Vol 7 (4) ◽  
pp. 659 ◽  
Author(s):  
RJ Aitken
Keyword(s):  
Reactive Oxygen Species ◽  
Lipid Peroxidation ◽  
Reactive Oxygen ◽  
Human Spermatozoa ◽  
Sperm Function ◽  
Oxygen Species ◽  
Normal Sperm ◽  
Oxidative Processes ◽  
Mammalian Spermatozoa

The cellular generation of reactive oxygen species was first observed in mammalian spermatozoa in the late 1940s. The field then remained dormant for 30 years until Thaddeus Mann and Roy Jones published a series of landmark papers in the 1970s in which the importance of lipid peroxidation as a mechanism for damaging mammalian spermatozoa was first intimated. The subsequent demonstration that human spermatozoa produce reactive oxygen species and are susceptible to peroxidative damage has triggered intense interest in the role of oxidative stress in the aetiology of male infertility. Moreover, data have recently been obtained to indicate that, although excessive exposure to reactive oxygen species may be harmful to spermatozoa, in physiological amounts these molecules are of importance in the control of normal sperm function. This review considers the dualistic role of reactive oxygen species and sets out the current understanding of the importance of oxidative processes in both the physiology and the pathology of the human spermatozoon. Extra keywords: human spermatozoa, reactive oxygen species.

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