Chemoprotective Effect of Leaf Extracts of Cecropia distachya Huber (Urticaceae) in Mice Submitted to Oxidative Stress Induced by Cyclophosphamide

The objective of this work was to evaluate the chemoprotective effects of the embaúba Cecropia distachya Huber (two methanolic fractions: F1 and F2) on oxidative stress induced by cyclophosphamide (75 mg kg-1) in mice, as well as phytochemical analyzes by LC-MS/MS. In the experimental model, the fractions increased the hepatic and cardiac catalase (CAT), reduced glutathione (GSH) of the kidney and the heart. F1 increased platelet levels (PLT), hemogram (RBC), hematocrit (HCT) and hemoglobin (Hb) and F1 reduced hepatic lipid peroxidation (TBARS) and aspartate aminotransferase (AST) activity increased. F1 was attributed to possible hypoglycemic activity and possible immunosuppressive effects and F2 presented antimutagenic activity. In some cases, the fractions were also hepatotoxic. These results demonstrated that the fractions stimulate the antioxidant defenses, being hypoglycemic (F1) and antimutagenic (F2), and, the harmful effects attributed to the fractions may be the association of compounds that were not elucidated in this work.

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Oxidative stress in dogs

Semina Ciências Agrárias ◽

10.5433/1679-0359.2016v37n3p1431 ◽

2016 ◽

Vol 37 (3) ◽

pp. 1431 ◽

Cited By ~ 4

Author(s):

Claudia Russo ◽

Ana Paula F. Rodrigues Loureiro Bracarense

Keyword(s):

Oxidative Stress ◽

Lipid Peroxidation ◽

Free Radicals ◽

Cell Membrane ◽

The Body ◽

Antioxidant Defenses ◽

Cellular Respiration ◽

Bodily Fluids ◽

Cellular Components ◽

Harmful Effects

Reactive oxygen species (ROS), also known as free radicals, are generated during cellular respiration. Under normal conditions, the body has the ability to neutralize the effects of free radicals by using its antioxidant defenses. In the case of an imbalance between oxidants and antioxidants, free radical production exceeds the capacity of organic combustion, resulting in oxidative stress. Of all the cellular components compromised by the harmful effects of ROS, the cell membrane is the most severely affected owing to lipid peroxidation, which invariably leads to changes in the membrane structure and permeability. With lipid peroxidation of the cell membrane, some by-products can be detected and measured in tissues, blood, and other bodily fluids. The measurement of biomarkers of oxidative stress is commonly used to quantify lipid peroxidation of the cell membrane in humans, a species in which ROS can be considered as a cause or consequence of oxidative stress-related diseases. In dogs, few studies have demonstrated this correlation. The present review aims to identify current literature knowledge relating to oxidative stress diseases and their detection in dogs.

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Oxidative stress and antioxidant defenses in mild cognitive impairment: a systematic review and meta-analysis.

10.1101/2021.11.22.21266698 ◽

2021 ◽

Author(s):

gallayaporn nantachai ◽

Asara Vasupanrajit ◽

Chavit Tunvirachaisakul ◽

Marco Solmi ◽

Michael Maes

Keyword(s):

Oxidative Stress ◽

Lipid Peroxidation ◽

Cognitive Impairment ◽

Mild Cognitive Impairment ◽

Web Of Science ◽

Reduced Glutathione ◽

Meta Analysis ◽

Antioxidant Defenses ◽

Healthy Controls ◽

Standardized Mean Difference

This study aims to systematically review and meta-analyze the nitro-oxidative stress (O&NS)/antioxidant (ANTIOX) ratio in the peripheral blood of people with mild cognitive impairment (MCI). We searched PubMed, Scopus, Google Scholar, and Web of Science for articles published from inception until July 31, 2021. Forty-six studies on 3.798 MCI individuals and 6.063 healthy controls were included. The O&NS/ANTIOX ratio was significantly higher in MCI than in controls with a Standardized Mean Difference (SMD)=0.378 (95% CI: 0.250; 0.506). MCI individuals showed increased lipid peroxidation (SMD=0.774, 95%CI: 4.416; 1.132) and O&NS-associated toxicity (SMD=0.621, CI: 0.377; 0.865) and reduced glutathione (GSH) defenses (SMD=0.725, 95%CI: 0.269; 1.182) as compared with controls. MCI was also accompanied by significantly increased homocysteine (SMD=0.320, CI: 0.059; 0.581), but not protein oxidation, and lowered non-vitamin (SMD=0.347, CI: 0.168; 0.527) and vitamin (SMD=0.564, CI: 0.129; 0.999) antioxidant defenses. The results show that MCI is at least in part due to increased neuro-oxidative toxicity and suggest that treatments targeting lipid peroxidation and the GSH system may be used to treat or prevent MCI.

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Oxidative Stress and Antioxidant Defenses in Mild Cognitive Impairment: A Systematic Review and Meta-Analysis

10.20944/preprints202111.0432.v1 ◽

2021 ◽

Author(s):

Gallayaporn Nantachai ◽

Asara Vasupanrajit ◽

Chavit Tunvirachaisakul ◽

Marco Solmi ◽

Michael Maes Michael Maes

Keyword(s):

Oxidative Stress ◽

Lipid Peroxidation ◽

Cognitive Impairment ◽

Mild Cognitive Impairment ◽

Web Of Science ◽

Reduced Glutathione ◽

Meta Analysis ◽

Antioxidant Defenses ◽

Healthy Controls ◽

Standardized Mean Difference

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Oxidative Stress in Rats After 60 Days of Hypergalactosemia or Hyperglycemia

International Journal of Toxicology ◽

10.1177/109158180302200603 ◽

2003 ◽

Vol 22 (6) ◽

pp. 423-427 ◽

Cited By ~ 17

Author(s):

Mary Otsyula ◽

Matthew S. King ◽

Tonya G. Ketcham ◽

Ruth A. Sanders ◽

John B. Watkins

Keyword(s):

Oxidative Stress ◽

Lipid Peroxidation ◽

Superoxide Dismutase ◽

Glutathione Peroxidase ◽

Insulin Treatment ◽

Diabetic Rats ◽

Diabetic Rat ◽

Glutathione Disulfide ◽

Hepatic Lipid Peroxidation ◽

Streptozotocin Diabetic Rats

Two of the models used in current diabetes research include the hypergalactosemic rat and the hyperglucosemic, streptozotocin-induced diabetic rat. Few studies, however, have examined the concurrence of these two models regarding the effects of elevated hexoses on biomarkers of oxidative stress. This study compared the activities of superoxide dismutase, catalase, glutathione peroxidase, and glutathione reductase and the concentrations of glutathione, glutathione disulfide, and thiobarbituric acid reactants (as a measure of lipid peroxidation) in liver, kidney, and heart of Sprague-Dawley rats after 60 days of either a 50% galactose diet or insulin deficiency caused by streptozotocin injection. Most rats from both models developed bilateral cataracts. Blood glucose and glycosy-lated hemoglobin A1c concentrations were elevated in streptozotocin diabetic rats. Streptozotocin diabetic rats exhibited elevated activities of renal superoxide dismutase, cardiac catalase, and renal and cardiac glutathione peroxidase, as well as elevated hepatic lipid peroxidation. Insulin treatment of streptozotocin-induced diabetic rats normalized altered markers. In galactosemic rats, hepatic lipid peroxidation was increased whereas glutathione reductase activity was diminished. Glutathione levels in liver were decreased in diabetic rats but elevated in the galactosemic rats, whereas hepatic glutathione disulfide concentrations were decreased much more in diabetes than in galactosemia. Insulin treatment reversed/prevented all changes caused by streptozotocin-induced diabetes. Lack of concomitance in these data indicate that the 60-day galactose-fed rat is not experiencing the same oxidative stress as the streptozotocin diabetic rat, and that investigators must be cautious drawing conclusions regarding the concurrence of the effects of the two animal models on oxidative stress biomarkers.

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Nose-only water-pipe smoking effects on airway resistance, inflammation, and oxidative stress in mice

Journal of Applied Physiology ◽

10.1152/japplphysiol.00194.2013 ◽

2013 ◽

Vol 115 (9) ◽

pp. 1316-1323 ◽

Cited By ~ 19

Author(s):

Abderrahim Nemmar ◽

Haider Raza ◽

Priya Yuvaraju ◽

Sumaya Beegam ◽

Annie John ◽

...

Keyword(s):

Oxidative Stress ◽

Lipid Peroxidation ◽

Airway Resistance ◽

Reduced Glutathione ◽

Mechanistic Explanation ◽

The United States ◽

Forced Oscillation Technique ◽

Water Pipe ◽

Respiratory Effects ◽

And Oxidative Stress

Water-pipe smoking (WPS) is a common practice in the Middle East and is now gaining popularity in Europe and the United States. However, there is a limited number of studies on the respiratory effects of WPS. More specifically, the underlying pulmonary pathophysiological mechanisms related to WPS exposure are not understood. Presently, we assessed the respiratory effects of nose-only exposure to mainstream WPS generated by commercially available honey flavored “moasel ” tobacco. The duration of the session was 30 min/day and 5 days/wk for 1 mo. Control mice were exposed to air only. Here, we measured in BALB/c mice the airway resistance using forced-oscillation technique. Lung inflammation was assessed histopathologically and by biochemical analysis of bronchoalveolar lavage (BAL) fluid, and oxidative stress was evaluated biochemically by measuring lipid peroxidation, reduced glutathione and several antioxidant enzymes. Pulmonary inflammation assessment showed an increase in neutrophil and lymphocyte numbers. Likewise, airway resistance was significantly increased in the WPS group compared with controls. Tumor necrosis factor α and interleukin 6 concentrations were significantly increased in BAL fluid. Lipid peroxidation in lung tissue was significantly increased whereas the level and activity of antioxidants including reduced glutathione, glutathione S transferase, and superoxide dismutase were all significantly decreased following WPS exposure, indicating the occurrence of oxidative stress. Moreover, carboxyhemoglobin levels were significantly increased in the WPS group. We conclude that 1-mo nose-only exposure to WPS significantly increased airway resistance, inflammation, and oxidative stress. Our results provide a mechanistic explanation for the limited clinical studies that reported the detrimental respiratory effects of WPS.

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

Brazilian Journal of Pharmaceutical Sciences ◽

10.1590/s1984-82502012000400009 ◽

2012 ◽

Vol 48 (4) ◽

pp. 659-665 ◽

Cited By ~ 2

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.

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The subchronic effects of 3,4-methylendioxymethamphetamine on oxidative stress in rat brain

Archives of Biological Sciences ◽

10.2298/abs1403075s ◽

2014 ◽

Vol 66 (3) ◽

pp. 1075-1081

Author(s):

Ivan Simic ◽

Violeta Iric-Cupic ◽

Rada Vucic ◽

Marina Petrovic ◽

Violeta Mladenovic ◽

...

Keyword(s):

Oxidative Stress ◽

Lipid Peroxidation ◽

Rat Brain ◽

Wistar Rats ◽

Superoxide Radical ◽

Reduced Glutathione ◽

Oxidative Stress Markers ◽

Sod Activity ◽

Stress Markers ◽

Male Wistar Rats

The aim of the present study was to evaluate the subchronic effects of 3,4-methylenedioxymethamphetamine on several oxidative stress markers: index of lipid peroxidation (ILP), superoxide dismutase (SOD) activity, superoxide radical (O2.-) levels, and reduced glutathione (GSH) levels in the frontal cortex, striatum and hippocampus of the rat. The study included 64 male Wistar rats (200-250g). The animals were treated per os with of 5, 10, or 20 mg/kg of 3,4-methylenedioxymethamphetamine (MDMA) every day for 15 days. The subchronic administration of MDMA resulted in an increase in ILP, SOD and O2.-, and a decrease in GSH, from which we conclude that oxidative stress was induced in rat brain.

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Combined Treatment with Sodium-Glucose Cotransporter-2 Inhibitor (Canagliflozin) and Dipeptidyl Peptidase-4 Inhibitor (Teneligliptin) Alleviates NASH Progression in A Non-Diabetic Rat Model of Steatohepatitis

International Journal of Molecular Sciences ◽

10.3390/ijms21062164 ◽

2020 ◽

Vol 21 (6) ◽

pp. 2164

Author(s):

Takahiro Ozutsumi ◽

Tadashi Namisaki ◽

Naotaka Shimozato ◽

Kosuke Kaji ◽

Yuki Tsuji ◽

...

Keyword(s):

Oxidative Stress ◽

Lipid Peroxidation ◽

Cell Proliferation ◽

Combined Treatment ◽

Diabetic Rat ◽

Hepatic Lipid ◽

Dipeptidyl Peptidase 4 ◽

Dipeptidyl Peptidase 4 Inhibitor ◽

Hepatic Lipid Peroxidation ◽

Diabetic Rat Model

Hepatocellular carcinoma (HCC) is the strongest independent predictor of mortality in non-alcoholic steatohepatitis (NASH)-related cirrhosis. The effects and mechanisms of combination of sodium-dependent glucose cotransporter inhibitor and canagliflozin (CA) and dipeptidyl peptidase-4 inhibitor and teneligliptin (TE) on non-diabetic NASH progression were examined. CA and TE suppressed choline-deficient, L-amino acid-defined diet-induced hepatic fibrogenesis and carcinogenesis. CA alone or with TE significantly decreased proinflammatory cytokine expression. CA and TE significantly attenuated hepatic lipid peroxidation. In vitro studies showed that TE alone or with CA inhibited cell proliferation and TGF-β1 and α1 (I)-procollagen mRNA expression in Ac-HSCs. CA+TE inhibited liver fibrogenesis by attenuating hepatic lipid peroxidation and inflammation and by inhibiting Ac-HSC proliferation with concomitant attenuation of hepatic lipid peroxidation. Moreover, CA+TE suppressed in vivo angiogenesis and oxidative DNA damage. CA or CA+TE inhibited HCC cells and human umbilical vein endothelial cell (HUVEC) proliferation. CA+TE suppressed vascular endothelial growth factor expression and promoted increased E-cadherin expression in HUVECs. CA+TE potentially exerts synergistic effects on hepatocarcinogenesis prevention by suppressing HCC cell proliferation and angiogenesis and concomitantly reducing oxidative stress and by inhibiting angiogenesis with attenuation of oxidative stress. CA+TE showed chemopreventive effects on NASH progression compared with single agent in non-diabetic rat model of NASH, concurrent with Ac-HSC and HCC cell proliferation, angiogenesis oxidative stress, and inflammation. Both agents are widely, safely used in clinical practice; combined treatment may represent a potential strategy against NASH.

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Lipid peroxidation and antioxidants as biomarkers of tissue damage

Clinical Chemistry ◽

10.1093/clinchem/41.12.1819 ◽

1995 ◽

Vol 41 (12) ◽

pp. 1819-1828 ◽

Cited By ~ 970

Author(s):

J M Gutteridge

Keyword(s):

Oxidative Stress ◽

Lipid Peroxidation ◽

Tissue Damage ◽

Stress Proteins ◽

Hypochlorous Acid ◽

Oxidant Stress ◽

The Body ◽

Peroxyl Radicals ◽

Antioxidant Defenses ◽

Fenton Chemistry

Abstract Disturbance of the balance between the production of reactive oxygen species such as superoxide; hydrogen peroxide; hypochlorous acid; hydroxyl, alkoxyl, and peroxyl radicals; and antioxidant defenses against them produces oxidative stress, which amplifies tissue damage by releasing prooxidative forms of reactive iron that are able to drive Fenton chemistry and lipid peroxidation and by eroding away protective sacrificial antioxidants. The body has a hierarchy of defense strategies to deal with oxidative stress within different cellular compartments, and superimposed on these are gene-regulated defenses involving the heat-shock and oxidant stress proteins.

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